Zheng Wang1, Xiaoxi Wang2, Fei Cheng2, Xue Wen2, Shi Feng2, Fang Yu2, Hui Tang2, Zhengjin Liu3, Xiaodong Teng2. 1. Department of Neurology, Hangzhou Seventh People's Hospital, Hangzhou, People's Republic of China. 2. Department of Pathology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, People's Republic of China. 3. Department of Pathology, Zhongshan Hospital, Xiamen University, Xiamen, People's Republic of China.
Abstract
BACKGROUND: Glioma is a common intracranial malignant tumor with high rates of invasiveness and mortality. This study aimed to investigate the mechanism of rapamycin in glioma. METHODS: U118-MG cells were treated with and without rapamycin in vivo and then collected for RNA sequencing. Differentially expressed miRNAs (DEMs) were screened and verified. MiR-26a-5p was selected for functional verification, and the target gene of miR-26a-5p was identified. The effects of miR-26a-5p on cell proliferation, cell cycle, apoptosis, and autophagy were also investigated. RESULTS: In total, 58 up-regulated and 41 down-regulated DEMs were identified between rapamycin-treated and untreated U118-MG cells. MiR-26-5p levels were up-regulated in U118-MG cells treated with 12.5 μM rapamycin, and death-associated protein kinase 1 (DAPK1) expression, a direct miR-26a-5p target gene, was down-regulated. Rapamycin substantially inhibited cell proliferation and cell percentage in the S phase and promoted cell apoptosis; miR-26a-5p inhibitor increased cell proliferation and cell cycle and decreased cell apoptosis; DAPK1 overexpression further induced cell proliferation, increased the cell number in the S phase, and inhibited apoptosis in glioma cells. Notably, rapamycin increased the autophagy-related Beclin1 protein expression levels and the LC3 II/I ratio. CONCLUSION: Rapamycin exerts anti-tumor effects by promoting autophagy in glioma cells, which was dependent on the miR-26a-5p/DAPK1 pathway activation by rapamycin.
BACKGROUND: Glioma is a common intracranial malignant tumor with high rates of invasiveness and mortality. This study aimed to investigate the mechanism of rapamycin in glioma. METHODS: U118-MG cells were treated with and without rapamycin in vivo and then collected for RNA sequencing. Differentially expressed miRNAs (DEMs) were screened and verified. MiR-26a-5p was selected for functional verification, and the target gene of miR-26a-5p was identified. The effects of miR-26a-5p on cell proliferation, cell cycle, apoptosis, and autophagy were also investigated. RESULTS: In total, 58 up-regulated and 41 down-regulated DEMs were identified between rapamycin-treated and untreated U118-MG cells. MiR-26-5p levels were up-regulated in U118-MG cells treated with 12.5 μM rapamycin, and death-associated protein kinase 1 (DAPK1) expression, a direct miR-26a-5p target gene, was down-regulated. Rapamycin substantially inhibited cell proliferation and cell percentage in the S phase and promoted cell apoptosis; miR-26a-5p inhibitor increased cell proliferation and cell cycle and decreased cell apoptosis; DAPK1 overexpression further induced cell proliferation, increased the cell number in the S phase, and inhibited apoptosis in glioma cells. Notably, rapamycin increased the autophagy-related Beclin1 protein expression levels and the LC3 II/I ratio. CONCLUSION: Rapamycin exerts anti-tumor effects by promoting autophagy in glioma cells, which was dependent on the miR-26a-5p/DAPK1 pathway activation by rapamycin.
As a common intracranial malignant tumor, glioma, caused by the carcinogenesis of glial cells originating in the neuroectoderm, has a high mortality.1 Early diagnosis and effective treatment are effective approaches to prevent further glioma deterioration.2 Recent studies have reported intensive progress in glioma treatment, including immunotherapy, sophisticated surgical resection and advanced chemoradiation.2,3 However, due to complex pathogenesis and higher recurrence, unsatisfactory prognosis and poor survival still exist.2 Therefore, it is essential to identify novel diagnostic and prognostic biomarkers and therapeutic targets, and to further elucidate the underlying molecular mechanisms of glioma.The DAPK family contains five kinases, namely DAPK1, DAPK 2, ZIPK, DRAK1, and DRAK2, among which DAPK1 is a Ca2/CaM-dependent Ser/Thr protein kinase.4 In 1995, Deiss et al discovered the DAPK1 gene through functional gene cloning technology when Hela cell death was induced with interferon-γ.5 This gene, located at chromosome 9q34.1, with a protein molecular weight of 160 kD, participates in many pathologic and physiologic processes including cell necrosis, apoptosis, and autophagy and is related to the biological activity of tumors.6–8It is well-known that the continuous updating of high-throughput sequencing and computer algorithms has revealed a large number of non-coding RNAs involved in various biological functions, including cell differentiation, apoptosis, migration, invasion, and proliferation in human diseases.9 MicroRNAs (miRNAs) are endogenous non-coding small-molecule RNAs that widely exist in several conditions.10 A growing number of studies have focused on and explored the functions of miRNAs in cancers.11 Previous studies have reported the abnormal expression of miRNAs in glioma and identified several miRNAs, including miRNA-204-5p,12 miRNA-637,13 miRNA-155,14 and miRNA-485-5p as diagnostic and prognostic biomarkers.15Rapamycin, also known as sirolimus, is a common inhibitor of mammalian target of rapamycin (mTOR).16 Hyperactivation of mTOR kinase usually occurs in various cancers and plays a critical role in cell growth, proliferation, autophagy and metabolism.17 Previous studies have demonstrated the tumor-inhibiting effect of rapamycin on glioma/glioblastoma.18–22 Rapamycin induces glioma stem/progenitor cell differentiation by activating autophagy.23 Yang et al showed suppressed growth and proliferation of human U87MG glioma cells by rapamycin combined with nimuatine, with cells arrested in the G1 phase.24 Moreover, rapamycin has been shown to promote autophagy and Beclin1 gene expression, increase the LC3 II/I ratio, and decrease P62 gene expression.25This study determined the effects of rapamycin on the proliferation, cell cycle, apoptosis, and autophagy of glioma cells, and whether the inhibitory effect of rapamycin on glioma cell growth may be related to the miR-26a-5p/DAPK1 pathway, which provides evidence for future studies of the mechanisms of action of rapamycin.
Materials and Methods
Cell Culture
Four glioma cell lines (U87, U118-MG, U251 and A172) were obtained from Shanghai Obio Technology Co., Ltd., and then maintained in complete DMEM medium (Hyclone) at 37 °C and 5% CO2.
CCK8 Assay
U87, U118-MG, U251, and A172 cells (5 × 103/each well) were grown in 96-well plates, respectively, and then exposed to rapamycin (Sigma) at different concentrations (0, 12.5, 50, 100, 150, 200, and 250 μM) for 12, 24, 48, and 72 h followed by the addition of 100 μL of CCK8 (Biosharp) for 1 h. Microplate spectrophotometer was used to evaluate cell viability based on the absorbance at 450 nm.
Western Blotting
U118-MG cells were exposed to 10 and 100 μM rapamycin for 0, 0.5, 1, 2, 4, 6, 12, 24, 48, and 72 h.Cells were then lysed by RIPA lysis buffer (Gibco), and proteins extracted using commercial kit (Pierce, Rockford, IL, USA). After being resolved visa SDS PAGE, protein samples were transferred to a PVDF membrane, which was blocked and reacted with DAPK1, LC3, Beclin1, or β-actin primary antibody (1:800, Abcam) overnight at 4 °C. After incubation with secondary antibody (1:5000, Abcam), protein levels were detected via enhanced chemiluminescence (Millipore, USA).
RNA Extraction and Sequencing
U118-MG cells were treated with 12.5 μM of rapamycin for 48 h. Cells were then collected, and total RNA isolated using RNAiso Plus (Takara, Shiga, Japan). RNA detection was carried out using a spectrophotometer (NanoDrop Technologies, Wilmington, Delaware, USA), and RNA with 2.0 < A260/A280 < 2.2 was used for subsequent RNA sequencing. Subsequently, TruSeq® Small RNA Library Prep Kit for Illumina® (New England Biolabs Inc., Beverly, MA, USA) was used to construct the RNA-seq library, with the Illumina Hiseq 2500 platform (Illumina, San Diego, CA, USA) used for sequencing.
Data Analysis
Data preprocessing was performed use the Oligo package (version 1.36.1, ) of R software, which mainly consisted of background correction, normalization and expression calculation. The classical Bayes method provided by the Limma package was employed to screen DEMs between control cells and cells treated with rapamycin. The p-value was estimated with the adjusted p-value (adj.p.value) was then determined based on the Benjamini & Hochberg method. Notably, the DEMs in this study were defined according to the cutoffs of p < 0.05 and |log fold change (FC)| > 0.5. Meanwhile, a Venn diagram was generated based on the obtained DEMs.
qRT-PCR Analysis
Total RNA was obtained using Trizol (Invitrogen) following the manufacturer’s instructions. ReverAid First Strand cDNA Synthesis Kit (Invitrogen) was used to obtain cDNA by RNA reverse transcription. qRT-PCR was carried out using SYBR Green qPCR Master Mix (Roche). PCR primers were: miR-143 sense primer 5ʹ-GGG GTG AGA TGA AGC ACT GTA GCT C-3ʹ and antisense primer 5ʹ-GGG GTA AGG CAC GCG GTG AAT GCC AA-3ʹ; miR-26a-5p sense primer 5ʹ-GGG GTT CAA GTA ATC CAG GA-3ʹ and antisense primer 5ʹ-TGC GTG TCG TGG AGT C-3ʹ; and U6 sense primer 5ʹ-CTC ACT TCG GCA GCA CAT A-3ʹ and antisense primer 5ʹ-AAC TCT TCA CGA TTT TGT CTG TC-3ʹ; U6 served as the internal control. Finally, miRNA expression data was evaluated by the 2−ΔΔCt method.
Luciferase Reporter Assay
Dual-luciferase activity assays were used to identify the targeted relationship between miR-26a-5p and DAPK1. The DAPK1 3ʹ-UTR-wild-type (WT) or mutant (MUT) were cloned into a pGL3 vector, and named DAPK1-WT, and DAPK1-MUT, respectively. MiR-26a-5p mimic or mimic control was co-transfected with DAPK1-WT or DAPK1-MUT into 293T cells, respectively, for 48 h using Lipofectamine 2000. Luciferase activity measurements were carried out using the Dual-Glo Luciferase Assay System (Promega).
Cell Transient Transfection and Treatment
MiR-26a-5p inhibitor, inhibitor NC, DAPK1 overexpression vector (pc-DAPK1), and pcDNA3.1 were provided by Jirui Technology CO., Ltd. (Shanghai, China). To evaluate the effect of miR-26a-5p on rapamycin-treated U118-MG cells, U118-MG cells were grown in 6-well plates for 24 h, and then transiently transfected with the above vectors using Lipofectamine 3000 (Thermo). Following 24 h of transfection, cells were treated with 12.5 μM rapamycin for 48 h.
Ethynyldeoxyuridine (EdU) Assay
The EdU kit (Invitrogen) was used for cell proliferation detection. Specifically, transfected U118-MG cells were incubated with 12.5 μM rapamycin and 10 μM EdU for 48 h, followed by cell collection and rinsing with PBS. Following treatment with 4% paraformaldehyde to fix cells for 15 min away from light, cells were incubated with working solution for 30 min. A flow cytometer (BD, CA, USA) was used to calculate the percentage of EdU-positive cells.
Flow Cytometry Assay
Cell cycle and apoptosis were evaluated by flow cytometry. Cells from various treatments were digested with trypsin and harvested. For cell cycle assays, cells were incubated on ice in 70% ethanol for 2 h and then stained with propidium iodide (PI) for 30 min at 37 °C in the dark. Apoptosis was detected according to instructions of the FITC-Annexin V Apoptosis kit (BD, CA, USA). A flow cytometer (BD, CA, USA) was used to measure the cell cycle and calculate the apoptotic cells numbers.
Statistical Analysis
Values are expressed as mean ± SD from three independent experiments. And the SPSS software was used for one-way analysis of variance followed by multiple comparisons, and p < 0.05 and P < 0.01 were considered the threshold for significant difference and very significant difference, respectively.
Results
Effect of Rapamycin on Different Glioma Cell
Four glioma cells (U87, U118-MG, U251, and A172 cells) were exposed to different rapamycin concentrations. CCK8 assay showed that rapamycin inhibited the cell viability of U118-MG and U87 cells at 24, 48 and 72 hours, and at 48 and 72 hours, respectively, (Figure 1A). A172 and U251 cell viability was not dose-dependent upon rapamycin treatment (). U87 and U118-MG cell treatment with different concentrations of rapamycin (10 and 100 μM), respectively, and Western blotting showed that rapamycin treatment decreased DAPK1 and P62 expression, and elevated the LC3 II/I ratio in U118-MG and U87 cells (). Furthermore, for U118-MG cells treated with increased rapamycin concentration for 72 h, results showed that 150–250 μM rapamycin treatment caused massive cell death, with P62 expression was obviously reduced after treatment with 12.5 μM rapamycin (Figure 1B). The 12.5 μM rapamycin concentration was selected to treat U118-MG cells for 48 h for microRNA second-generation sequencing.
Figure 1
Rapamycin effect on U118-MG and U87 cells. (A) Viability of U118-MG and U87 cells treated with different rapamycin for 12, 24, 48, and 72 h assessed via CCK-8 assay. (B) DAPK1 and P62 expression in U118-MG cells treated with different rapamycin concentrations analyzed via Western blotting.
Rapamycin effect on U118-MG and U87 cells. (A) Viability of U118-MG and U87 cells treated with different rapamycin for 12, 24, 48, and 72 h assessed via CCK-8 assay. (B) DAPK1 and P62 expression in U118-MG cells treated with different rapamycin concentrations analyzed via Western blotting.
Sequencing Data Analysis and Verification
As shown in the Venn diagram (Figure 2A), 99 DEMs between U118-MG cells treated with and without 12.5 μM rapamycin, including 58 up-regulated DEMs and 41 down-regulated DEMs, were screened according to the methods described above. Hsa-mir-143-3p, hsa-miR-124-3p, and hsa-miR-26a-5p were then selected for verification via RT-qPCR. Results revealed that after 12.5 μMrapamycin treatment for 48 h, hsa-miR-143-3p and hsa-miR-26a-5p levels were up-regulated, however, hsa-miR-124-3p could not be detected (Figure 2B). Hsa-miR-26-5p was selected for functional verification in subsequent experiments.
Figure 2
Bioinformatics analysis and verification. (A) Venn diagram showing differentially expressed miRNAs between U118-MG cells treated with and without 12.5 μM rapamycin. (B) Hsa-mir-143-3p and hsa-miR-26a-5p levels in U118-MG cells treated with or without 12.5 μM rapamycin analyzed via RT-qPCR. At least three repeats were conducted, and the mean ± SD is presented, **P<0.01.
Bioinformatics analysis and verification. (A) Venn diagram showing differentially expressed miRNAs between U118-MG cells treated with and without 12.5 μM rapamycin. (B) Hsa-mir-143-3p and hsa-miR-26a-5p levels in U118-MG cells treated with or without 12.5 μM rapamycin analyzed via RT-qPCR. At least three repeats were conducted, and the mean ± SD is presented, **P<0.01.
DAPK1 Was Verified as a Functional Target of miR-26a-5p
DAPK1 was considered a potential target gene of miR-26a-5p according to TargetScan databases (Figure 3A). Luciferase receptor assay showed that after co-transfection with DAPK1-WT and miR-26a-5p mimic, the luciferase activity was reduced compared to co-transfection with mimic control, where no significant difference was found after DAPK1-MUT treatment (Figure 3B), suggesting that DAPK1 is a direct miR-26a-5p target gene.
Figure 3
MiR-26a-5p target gene identification. (A) Prediction of the binding site of miR-26a-5p and death associated protein kinase 1 (DAPK1) using the TargetScan database; (B) target regulation of miR-26a-5p to DAPK1 proved by luciferase reporter system. At least three repeats were conducted, and the mean ± SD is presented, **P<0.01.
MiR-26a-5p target gene identification. (A) Prediction of the binding site of miR-26a-5p and death associated protein kinase 1 (DAPK1) using the TargetScan database; (B) target regulation of miR-26a-5p to DAPK1 proved by luciferase reporter system. At least three repeats were conducted, and the mean ± SD is presented, **P<0.01.
Effect of Rapamycin on Cell Proliferation, Cell Cycle and Apoptosis in Glioma Cells
The Edu assay showed that rapamycin significantly inhibited cell proliferation, and the addition of a miR26a inhibitor increased cell proliferation, whereas the addition of pc-DAPK1 significantly promoted cell proliferation (Figure 4A). Cell cycle analysis results showed that rapamycin significantly inhibited the number of S phase cells, whereas the addition of pc-DAPK1 significantly increased the number of S phase cells (Figure 4B). Additionally, rapamycin treatment promoted apoptosis, while the addition of miR-26a-5p inhibitor inhibited apoptosis, and the overexpression of DAPK1 further decreased the number of apoptotic cells (Figure 4C).
Figure 4
Rapamycin effect on cell proliferation, cell cycle and apoptosis in glioma cells. (A) Cell proliferation in U118-MG and U87 cells co-treated with rapamycin, miR-26a-5p inhibitor, and/or pc-DAPK1 assessed via Ethynyldeoxyuridine assay. (B) Cell cycle of U118-MG and U87 cells co-treated with rapamycin, miR-26a-5p inhibitor, and/or pc-death associated protein kinase 1 (DAPK1) analyzed via flow cytometry assay. (C) Apoptosis of U118-MG and U87 cells co-treated with rapamycin, miR-26a-5p inhibitor, and/or pc-DAPK1 detected using flow cytometry assay. At least three repeats were conducted, and the mean ± SD is presented, *P<0.05, **P<0.01.
Rapamycin effect on cell proliferation, cell cycle and apoptosis in glioma cells. (A) Cell proliferation in U118-MG and U87 cells co-treated with rapamycin, miR-26a-5p inhibitor, and/or pc-DAPK1 assessed via Ethynyldeoxyuridine assay. (B) Cell cycle of U118-MG and U87 cells co-treated with rapamycin, miR-26a-5p inhibitor, and/or pc-death associated protein kinase 1 (DAPK1) analyzed via flow cytometry assay. (C) Apoptosis of U118-MG and U87 cells co-treated with rapamycin, miR-26a-5p inhibitor, and/or pc-DAPK1 detected using flow cytometry assay. At least three repeats were conducted, and the mean ± SD is presented, *P<0.05, **P<0.01.
Effect of Rapamycin on Cell Autophagy in Glioma Cells
When U118-MG cells were treated with rapamycin, miR-26a-5p inhibitor and/or pc-DAPK1 for 48 h, RT-qPCR showed that miR-26a-5p levels were significantly increased after treatment with rapamycin, whereas miR-26a-5p levels were significantly inhibited by the miR-26a-5p inhibitor (Figure 5A). However, DAPK1 mRNA expression levels decreased significantly after rapamycin treatment, increasing significantly with the addition of miR-26a-5p inhibitor and pc-DAPK1 (Figure 5B). Additionally, Western blotting showed that after treatment with rapamycin, DAPK1 protein expression levels decreased significantly, whereas Beclin1 protein expression levels and LC3 II/I ratio increased significantly (Figure 5C). Additionally, to further verify that rapamycin can promote glioma cell autophagy, an immunofluorescence assay was used to detect LC3 expression. Results showed that rapamycin promoted glioma cell autophagy through the miR-26a-5p/DAPK1 signaling pathway (Figure 5D).
Figure 5
Rapamycin effect on cell autophagy in glioma cells. (A) MiR-26a-5p levels in U118-MG and U87 cells co-treated with rapamycin, miR-26a-5p inhibitor, and/or pc-DAPK1 for 48 h detected using RT-qPCR. (B) DAPK1 mRNA levels in U118-MG and U87 cells co-treated with rapamycin, miR-26a-5p inhibitor, and/or pc-DAPK1 for 48 h detected using RT-qPCR. (C) DAPK1 protein expression, Beclin1, and LC3 levels in U118-MG and U87 cells co-treated with rapamycin, miR-26a-5p inhibitor, and/or pc-DAPK1 detected using Western blotting. (D) Immunofluorescence detection of LC3 protein expression. At least three repeats were conducted, and the mean ± SD is presented, *P<0.05, **P<0.01.
Rapamycin effect on cell autophagy in glioma cells. (A) MiR-26a-5p levels in U118-MG and U87 cells co-treated with rapamycin, miR-26a-5p inhibitor, and/or pc-DAPK1 for 48 h detected using RT-qPCR. (B) DAPK1 mRNA levels in U118-MG and U87 cells co-treated with rapamycin, miR-26a-5p inhibitor, and/or pc-DAPK1 for 48 h detected using RT-qPCR. (C) DAPK1 protein expression, Beclin1, and LC3 levels in U118-MG and U87 cells co-treated with rapamycin, miR-26a-5p inhibitor, and/or pc-DAPK1 detected using Western blotting. (D) Immunofluorescence detection of LC3 protein expression. At least three repeats were conducted, and the mean ± SD is presented, *P<0.05, **P<0.01.
Discussion
Glioma is a primary brain tumor that seriously affects human health. DAPK1 has been confirmed to be related to glioma cell activity, meaning DAPK1 may be a target for glioma therapy. DAPK1, calcium/calmodulin-regulated serine/threonine kinase, plays key roles in mediating cell apoptosis and autophagy.26 Autophagy is a lysosomal-mediated process involved in cell growth, differentiation, viability and other pathological and physiological processes.27 It degrades damaged intracellular organelles, abnormal protein and other substances deposition, and maintains cellular homeostasis.28 Therefore, autophagy is a conservative in vivo system that plays a dual role in tumor occurrence and development.29Few studies have focused on the illuminating mechanism of action of rapamycin in glioma cell via bioinformatics analyses. Additionally, accumulating evidence has indicated a generally low miR-26a-5p expression in several cancers, including bladder cancer,30 colorectal carcinoma,31 prostate cancer,32 and lung cancer,33 whereas high miR-26a-5p expression levels can inhibit tumor growth. In the present study, we found that 58 DEMs were up-regulated and 41 DEMs were down-regulated in rapamycin-treated U118-MG cells based on bioinformatics analysis. MiR-26-5p was proved to be highly expressed in U118-MG cells treated with 12.5 μM rapamycin. Additionally, studies have shown that rapamycin can inhibit cell proliferation, arrest the cell cycle in the G1 phase, and promote apoptosis.20–22 In this study, rapamycin inhibited cell proliferation and the number of cells in S phase and promoted apoptosis; the addition of miR-26a-5p inhibitor reduced the rapamycin effect on inhibiting cell proliferation, stagnated the cell cycle in S phase, promoting apoptosis, and increased Beclin1 protein expression levels and LC3 II/I ratio. Therefore, rapamycin may inhibit glioma cell growth by up-regulating miR-26a-5p expression.Studies have confirmed that Beclin1 and LC3 II/I ratio are indices of autophagy activity.34 This study demonstrated that rapamycin could regulate Beclin1 and LC3 expression. Generally, more than 30 autophagy-related (ATG) genes are involved in every step of this process.34 Among them, microtubule associated protein1 light chain 3, a mammalian homolog of yeast Atg8, is considered a key regulator of autophagy, participating in several steps, including the growth of autophagic membranes, recognition of autophagic cargoes, and fusion of autophagosomes with lysosomes.35–37 LC3 is synthesized as a precursor form cleaved by the protease ATG4B, resulting in the cytosolic isoform LC3-I. In turn, LC3-I is conjugated to phosphatidylethanolamine to form LC3-II upon autophagy induction.38–40 LC3-II binds to the autophagosome membrane and remains bound to it until it is degraded in the autolysosomes. LC3-II is an important marker for assessing autophagy activity and is the only reliable autophagy marker to date.41 Therefore, in this study, LC3 protein expression was detected via immunofluorescence. Results showed that rapamycin increased LC3 expression, which further revealed that rapamycin could promote autophagy.Furthermore, DAPK1 was confirmed as the direct target gene of miR-26a-5p. MiR-26a-5p could reduce DAPK1expression, which could be attenuated by the addition of the miR-26a-5p inhibitor. Furthermore, rapamycin could up-regulate miR-26a-5p expression. Notably, rapamycin could also reduce DAPK1 expression and promote autophagy-related protein expression. Rapamycin treatment increased Beclin1 and LC3 II/I expression levels.
Conclusions
In this study, we found that miR-26a-5p was overexpressed in rapamycin-treated glioma cells, whereas DAPK1 expression was inhibited. Additionally, rapamycin may exert its antitumor effect by promoting autophagy depending on miR-26a-5p/DAPK1 pathway activation by rapamycin.
Authors: T Que; Y Song; Z Liu; S Zheng; H Long; Z Li; Y Liu; G Wang; Y Liu; J Zhou; X Zhang; W Fang; S Qi Journal: Oncogene Date: 2015-01-19 Impact factor: 9.867
Authors: Michael Weller; Wolfgang Wick; Ken Aldape; Michael Brada; Mitchell Berger; Stefan M Pfister; Ryo Nishikawa; Mark Rosenthal; Patrick Y Wen; Roger Stupp; Guido Reifenberger Journal: Nat Rev Dis Primers Date: 2015-07-16 Impact factor: 52.329
Authors: Daniel J Klionsky; Kotb Abdelmohsen; Akihisa Abe; Md Joynal Abedin; Hagai Abeliovich; Abraham Acevedo Arozena; Hiroaki Adachi; Christopher M Adams; Peter D Adams; Khosrow Adeli; Peter J Adhihetty; Sharon G Adler; Galila Agam; Rajesh Agarwal; Manish K Aghi; Maria Agnello; Patrizia Agostinis; Patricia V Aguilar; Julio Aguirre-Ghiso; Edoardo M Airoldi; Slimane Ait-Si-Ali; Takahiko Akematsu; Emmanuel T Akporiaye; Mohamed Al-Rubeai; Guillermo M Albaiceta; Chris Albanese; Diego Albani; Matthew L Albert; Jesus Aldudo; Hana Algül; Mehrdad Alirezaei; Iraide Alloza; Alexandru Almasan; Maylin Almonte-Beceril; Emad S Alnemri; Covadonga Alonso; Nihal Altan-Bonnet; Dario C Altieri; Silvia Alvarez; Lydia Alvarez-Erviti; Sandro Alves; Giuseppina Amadoro; Atsuo Amano; Consuelo Amantini; Santiago Ambrosio; Ivano Amelio; Amal O Amer; Mohamed Amessou; Angelika Amon; Zhenyi An; Frank A Anania; Stig U Andersen; Usha P Andley; Catherine K Andreadi; Nathalie Andrieu-Abadie; Alberto Anel; David K Ann; Shailendra Anoopkumar-Dukie; Manuela Antonioli; Hiroshi Aoki; Nadezda Apostolova; Saveria Aquila; Katia Aquilano; Koichi Araki; Eli Arama; Agustin Aranda; Jun Araya; Alexandre Arcaro; Esperanza Arias; Hirokazu Arimoto; Aileen R Ariosa; Jane L Armstrong; Thierry Arnould; Ivica Arsov; Katsuhiko Asanuma; Valerie Askanas; Eric Asselin; Ryuichiro Atarashi; Sally S Atherton; Julie D Atkin; Laura D Attardi; Patrick Auberger; Georg Auburger; Laure Aurelian; Riccardo Autelli; Laura Avagliano; Maria Laura Avantaggiati; Limor Avrahami; Suresh Awale; Neelam Azad; Tiziana Bachetti; Jonathan M Backer; Dong-Hun Bae; Jae-Sung Bae; Ok-Nam Bae; Soo Han Bae; Eric H Baehrecke; Seung-Hoon Baek; Stephen Baghdiguian; Agnieszka Bagniewska-Zadworna; Hua Bai; Jie Bai; Xue-Yuan Bai; Yannick Bailly; Kithiganahalli Narayanaswamy Balaji; Walter Balduini; Andrea Ballabio; Rena Balzan; Rajkumar Banerjee; Gábor Bánhegyi; Haijun Bao; Benoit Barbeau; Maria D Barrachina; Esther Barreiro; Bonnie Bartel; Alberto Bartolomé; Diane C Bassham; Maria Teresa Bassi; Robert C Bast; Alakananda Basu; Maria Teresa Batista; Henri Batoko; Maurizio Battino; Kyle Bauckman; Bradley L Baumgarner; K Ulrich Bayer; Rupert Beale; Jean-François Beaulieu; George R Beck; Christoph Becker; J David Beckham; Pierre-André Bédard; Patrick J Bednarski; Thomas J Begley; Christian Behl; Christian Behrends; Georg Mn Behrens; Kevin E Behrns; Eloy Bejarano; Amine Belaid; Francesca Belleudi; Giovanni Bénard; Guy Berchem; Daniele Bergamaschi; Matteo Bergami; Ben Berkhout; Laura Berliocchi; Amélie Bernard; Monique Bernard; Francesca Bernassola; Anne Bertolotti; Amanda S Bess; Sébastien Besteiro; Saverio Bettuzzi; Savita Bhalla; Shalmoli Bhattacharyya; Sujit K Bhutia; Caroline Biagosch; Michele Wolfe Bianchi; Martine Biard-Piechaczyk; Viktor Billes; Claudia Bincoletto; Baris Bingol; Sara W Bird; Marc Bitoun; Ivana Bjedov; Craig Blackstone; Lionel Blanc; Guillermo A Blanco; Heidi Kiil Blomhoff; Emilio Boada-Romero; Stefan Böckler; Marianne Boes; Kathleen Boesze-Battaglia; Lawrence H Boise; Alessandra Bolino; Andrea Boman; Paolo Bonaldo; Matteo Bordi; Jürgen Bosch; Luis M Botana; Joelle Botti; German Bou; Marina Bouché; Marion Bouchecareilh; Marie-Josée Boucher; Michael E Boulton; Sebastien G Bouret; Patricia Boya; Michaël Boyer-Guittaut; Peter V Bozhkov; Nathan Brady; Vania Mm Braga; Claudio Brancolini; Gerhard H Braus; José M Bravo-San Pedro; Lisa A Brennan; Emery H Bresnick; Patrick Brest; Dave Bridges; Marie-Agnès Bringer; Marisa Brini; Glauber C Brito; Bertha Brodin; Paul S Brookes; Eric J Brown; Karen Brown; Hal E Broxmeyer; Alain Bruhat; Patricia Chakur Brum; John H Brumell; Nicola Brunetti-Pierri; Robert J Bryson-Richardson; Shilpa Buch; Alastair M Buchan; Hikmet Budak; Dmitry V Bulavin; Scott J Bultman; Geert Bultynck; Vladimir Bumbasirevic; Yan Burelle; Robert E Burke; Margit Burmeister; Peter Bütikofer; Laura Caberlotto; Ken Cadwell; Monika Cahova; Dongsheng Cai; Jingjing Cai; Qian Cai; Sara Calatayud; Nadine Camougrand; Michelangelo Campanella; Grant R Campbell; Matthew Campbell; Silvia Campello; Robin Candau; Isabella Caniggia; Lavinia Cantoni; Lizhi Cao; Allan B Caplan; Michele Caraglia; Claudio Cardinali; Sandra Morais Cardoso; Jennifer S Carew; Laura A Carleton; Cathleen R Carlin; Silvia Carloni; Sven R Carlsson; Didac Carmona-Gutierrez; Leticia Am Carneiro; Oliana Carnevali; Serena Carra; Alice Carrier; Bernadette Carroll; Caty Casas; Josefina Casas; Giuliana Cassinelli; Perrine Castets; Susana Castro-Obregon; Gabriella Cavallini; Isabella Ceccherini; Francesco Cecconi; Arthur I Cederbaum; Valentín Ceña; Simone Cenci; Claudia Cerella; Davide Cervia; Silvia Cetrullo; Hassan Chaachouay; Han-Jung Chae; Andrei S Chagin; Chee-Yin Chai; Gopal Chakrabarti; Georgios Chamilos; Edmond Yw Chan; Matthew Tv Chan; Dhyan Chandra; Pallavi Chandra; Chih-Peng Chang; Raymond Chuen-Chung Chang; Ta Yuan Chang; John C Chatham; Saurabh Chatterjee; Santosh Chauhan; Yongsheng Che; Michael E Cheetham; Rajkumar Cheluvappa; Chun-Jung Chen; Gang Chen; Guang-Chao Chen; Guoqiang Chen; Hongzhuan Chen; Jeff W Chen; Jian-Kang Chen; Min Chen; Mingzhou Chen; Peiwen Chen; Qi Chen; Quan Chen; Shang-Der Chen; Si Chen; Steve S-L Chen; Wei Chen; Wei-Jung Chen; Wen Qiang Chen; Wenli Chen; Xiangmei Chen; Yau-Hung Chen; Ye-Guang Chen; Yin Chen; Yingyu Chen; Yongshun Chen; Yu-Jen Chen; Yue-Qin Chen; Yujie Chen; Zhen Chen; Zhong Chen; Alan Cheng; Christopher Hk Cheng; Hua Cheng; Heesun Cheong; Sara Cherry; Jason Chesney; Chun Hei Antonio Cheung; Eric Chevet; Hsiang Cheng Chi; Sung-Gil Chi; Fulvio Chiacchiera; Hui-Ling Chiang; Roberto Chiarelli; Mario Chiariello; Marcello Chieppa; Lih-Shen Chin; Mario Chiong; Gigi Nc Chiu; Dong-Hyung Cho; Ssang-Goo Cho; William C Cho; Yong-Yeon Cho; Young-Seok Cho; Augustine Mk Choi; Eui-Ju Choi; Eun-Kyoung Choi; Jayoung Choi; Mary E Choi; Seung-Il Choi; Tsui-Fen Chou; Salem Chouaib; Divaker Choubey; Vinay Choubey; Kuan-Chih Chow; Kamal Chowdhury; Charleen T Chu; Tsung-Hsien Chuang; Taehoon Chun; Hyewon Chung; Taijoon Chung; Yuen-Li Chung; Yong-Joon Chwae; Valentina Cianfanelli; Roberto Ciarcia; Iwona A Ciechomska; Maria Rosa Ciriolo; Mara Cirone; Sofie Claerhout; Michael J Clague; Joan Clària; Peter Gh Clarke; Robert Clarke; Emilio Clementi; Cédric Cleyrat; Miriam Cnop; Eliana M Coccia; Tiziana Cocco; Patrice Codogno; Jörn Coers; Ezra Ew Cohen; David Colecchia; Luisa Coletto; Núria S Coll; Emma Colucci-Guyon; Sergio Comincini; Maria Condello; Katherine L Cook; Graham H Coombs; Cynthia D Cooper; J Mark Cooper; Isabelle Coppens; Maria Tiziana Corasaniti; Marco Corazzari; Ramon Corbalan; Elisabeth Corcelle-Termeau; Mario D Cordero; Cristina Corral-Ramos; Olga Corti; Andrea Cossarizza; Paola Costelli; Safia Costes; Susan L Cotman; Ana Coto-Montes; Sandra Cottet; Eduardo Couve; Lori R Covey; L Ashley Cowart; Jeffery S Cox; Fraser P Coxon; Carolyn B Coyne; Mark S Cragg; Rolf J Craven; Tiziana Crepaldi; Jose L Crespo; Alfredo Criollo; Valeria Crippa; Maria Teresa Cruz; Ana Maria Cuervo; Jose M Cuezva; Taixing Cui; Pedro R Cutillas; Mark J Czaja; Maria F Czyzyk-Krzeska; Ruben K Dagda; Uta Dahmen; Chunsun Dai; Wenjie Dai; Yun Dai; Kevin N Dalby; Luisa Dalla Valle; Guillaume Dalmasso; Marcello D'Amelio; Markus Damme; Arlette Darfeuille-Michaud; Catherine Dargemont; Victor M Darley-Usmar; Srinivasan Dasarathy; Biplab Dasgupta; Srikanta Dash; Crispin R Dass; Hazel Marie Davey; Lester M Davids; David Dávila; Roger J Davis; Ted M Dawson; Valina L Dawson; Paula Daza; Jackie de Belleroche; Paul de Figueiredo; Regina Celia Bressan Queiroz de Figueiredo; José de la Fuente; Luisa De Martino; Antonella De Matteis; Guido Ry De Meyer; Angelo De Milito; Mauro De Santi; Wanderley de Souza; Vincenzo De Tata; Daniela De Zio; Jayanta Debnath; Reinhard Dechant; Jean-Paul Decuypere; Shane Deegan; Benjamin Dehay; Barbara Del Bello; Dominic P Del Re; Régis Delage-Mourroux; Lea Md Delbridge; Louise Deldicque; Elizabeth Delorme-Axford; Yizhen Deng; Joern Dengjel; Melanie Denizot; Paul Dent; Channing J Der; Vojo Deretic; Benoît Derrien; Eric Deutsch; Timothy P Devarenne; Rodney J Devenish; Sabrina Di Bartolomeo; Nicola Di Daniele; Fabio Di Domenico; Alessia Di Nardo; Simone Di Paola; Antonio Di Pietro; Livia Di Renzo; Aaron DiAntonio; Guillermo Díaz-Araya; Ines Díaz-Laviada; Maria T Diaz-Meco; Javier Diaz-Nido; Chad A Dickey; Robert C Dickson; Marc Diederich; Paul Digard; Ivan Dikic; Savithrama P Dinesh-Kumar; Chan Ding; Wen-Xing Ding; Zufeng Ding; Luciana Dini; Jörg Hw Distler; Abhinav Diwan; Mojgan Djavaheri-Mergny; Kostyantyn Dmytruk; Renwick Cj Dobson; Volker Doetsch; Karol Dokladny; Svetlana Dokudovskaya; Massimo Donadelli; X Charlie Dong; Xiaonan Dong; Zheng Dong; Terrence M Donohue; Kelly S Doran; Gabriella D'Orazi; Gerald W Dorn; Victor Dosenko; Sami Dridi; Liat Drucker; Jie Du; Li-Lin Du; Lihuan Du; André du Toit; Priyamvada Dua; Lei Duan; Pu Duann; Vikash Kumar Dubey; Michael R Duchen; Michel A Duchosal; Helene Duez; Isabelle Dugail; Verónica I Dumit; Mara C Duncan; Elaine A Dunlop; William A Dunn; Nicolas Dupont; Luc Dupuis; Raúl V Durán; Thomas M Durcan; Stéphane Duvezin-Caubet; Umamaheswar Duvvuri; Vinay Eapen; Darius Ebrahimi-Fakhari; Arnaud Echard; Leopold Eckhart; Charles L Edelstein; Aimee L Edinger; Ludwig Eichinger; Tobias Eisenberg; Avital Eisenberg-Lerner; N Tony Eissa; Wafik S El-Deiry; Victoria El-Khoury; Zvulun Elazar; Hagit Eldar-Finkelman; Chris Jh Elliott; Enzo Emanuele; Urban Emmenegger; Nikolai Engedal; Anna-Mart Engelbrecht; Simone Engelender; Jorrit M Enserink; Ralf Erdmann; Jekaterina Erenpreisa; Rajaraman Eri; Jason L Eriksen; Andreja Erman; Ricardo Escalante; Eeva-Liisa Eskelinen; Lucile Espert; Lorena Esteban-Martínez; Thomas J Evans; Mario Fabri; Gemma Fabrias; Cinzia Fabrizi; Antonio Facchiano; Nils J Færgeman; Alberto Faggioni; W Douglas Fairlie; Chunhai Fan; Daping Fan; Jie Fan; Shengyun Fang; Manolis Fanto; Alessandro Fanzani; Thomas Farkas; Mathias Faure; Francois B Favier; Howard Fearnhead; Massimo Federici; Erkang Fei; Tania C Felizardo; Hua Feng; Yibin Feng; Yuchen Feng; Thomas A Ferguson; Álvaro F Fernández; Maite G Fernandez-Barrena; Jose C Fernandez-Checa; Arsenio Fernández-López; Martin E Fernandez-Zapico; Olivier Feron; Elisabetta Ferraro; Carmen Veríssima Ferreira-Halder; Laszlo Fesus; Ralph Feuer; Fabienne C Fiesel; Eduardo C Filippi-Chiela; Giuseppe Filomeni; Gian Maria Fimia; John H Fingert; Steven Finkbeiner; Toren Finkel; Filomena Fiorito; Paul B Fisher; Marc Flajolet; Flavio Flamigni; Oliver Florey; Salvatore Florio; R Andres Floto; Marco Folini; Carlo Follo; Edward A Fon; Francesco Fornai; Franco Fortunato; Alessandro Fraldi; Rodrigo Franco; Arnaud Francois; Aurélie François; Lisa B Frankel; Iain Dc Fraser; Norbert Frey; Damien G Freyssenet; Christian Frezza; Scott L Friedman; Daniel E Frigo; Dongxu Fu; José M Fuentes; Juan Fueyo; Yoshio Fujitani; Yuuki Fujiwara; Mikihiro Fujiya; Mitsunori Fukuda; Simone Fulda; Carmela Fusco; Bozena Gabryel; Matthias Gaestel; Philippe Gailly; Malgorzata Gajewska; Sehamuddin Galadari; Gad Galili; Inmaculada Galindo; Maria F Galindo; Giovanna Galliciotti; Lorenzo Galluzzi; Luca Galluzzi; Vincent Galy; Noor Gammoh; Sam Gandy; Anand K Ganesan; Swamynathan Ganesan; Ian G Ganley; Monique Gannagé; Fen-Biao Gao; Feng Gao; Jian-Xin Gao; Lorena García Nannig; Eleonora García Véscovi; Marina Garcia-Macía; Carmen Garcia-Ruiz; Abhishek D Garg; Pramod Kumar Garg; Ricardo Gargini; Nils Christian Gassen; Damián Gatica; Evelina Gatti; Julie Gavard; Evripidis Gavathiotis; Liang Ge; Pengfei Ge; Shengfang Ge; Po-Wu Gean; Vania Gelmetti; Armando A Genazzani; Jiefei Geng; Pascal Genschik; Lisa Gerner; Jason E Gestwicki; David A Gewirtz; Saeid Ghavami; Eric Ghigo; Debabrata Ghosh; Anna Maria Giammarioli; Francesca Giampieri; Claudia Giampietri; Alexandra Giatromanolaki; Derrick J Gibbings; Lara Gibellini; Spencer B Gibson; Vanessa Ginet; Antonio Giordano; Flaviano Giorgini; Elisa Giovannetti; Stephen E Girardin; Suzana Gispert; Sandy Giuliano; Candece L Gladson; Alvaro Glavic; Martin Gleave; Nelly Godefroy; Robert M Gogal; Kuppan Gokulan; Gustavo H Goldman; Delia Goletti; Michael S Goligorsky; Aldrin V Gomes; Ligia C Gomes; Hernando Gomez; Candelaria Gomez-Manzano; Rubén Gómez-Sánchez; Dawit Ap Gonçalves; Ebru Goncu; Qingqiu Gong; Céline Gongora; Carlos B Gonzalez; Pedro Gonzalez-Alegre; Pilar Gonzalez-Cabo; Rosa Ana González-Polo; Ing Swie Goping; Carlos Gorbea; Nikolai V Gorbunov; Daphne R Goring; Adrienne M Gorman; Sharon M Gorski; Sandro Goruppi; Shino Goto-Yamada; Cecilia Gotor; Roberta A Gottlieb; Illana Gozes; Devrim Gozuacik; Yacine Graba; Martin Graef; Giovanna E Granato; Gary Dean Grant; Steven Grant; Giovanni Luca Gravina; Douglas R Green; Alexander Greenhough; Michael T Greenwood; Benedetto Grimaldi; Frédéric Gros; Charles Grose; Jean-Francois Groulx; Florian Gruber; Paolo Grumati; Tilman Grune; Jun-Lin Guan; Kun-Liang Guan; Barbara Guerra; Carlos Guillen; Kailash Gulshan; Jan Gunst; Chuanyong Guo; Lei Guo; Ming Guo; Wenjie Guo; Xu-Guang Guo; Andrea A Gust; Åsa B Gustafsson; Elaine Gutierrez; Maximiliano G Gutierrez; Ho-Shin Gwak; Albert Haas; James E Haber; Shinji Hadano; Monica Hagedorn; David R Hahn; Andrew J Halayko; Anne Hamacher-Brady; Kozo Hamada; Ahmed Hamai; Andrea Hamann; Maho Hamasaki; Isabelle Hamer; Qutayba Hamid; Ester M Hammond; Feng Han; Weidong Han; James T Handa; John A Hanover; Malene Hansen; Masaru Harada; Ljubica Harhaji-Trajkovic; J Wade Harper; Abdel Halim Harrath; Adrian L Harris; James Harris; Udo Hasler; Peter Hasselblatt; Kazuhisa Hasui; Robert G Hawley; Teresa S Hawley; Congcong He; Cynthia Y He; Fengtian He; Gu He; Rong-Rong He; Xian-Hui He; You-Wen He; Yu-Ying He; Joan K Heath; Marie-Josée Hébert; Robert A Heinzen; Gudmundur Vignir Helgason; Michael Hensel; Elizabeth P Henske; Chengtao Her; Paul K Herman; Agustín Hernández; Carlos Hernandez; Sonia Hernández-Tiedra; Claudio Hetz; P Robin Hiesinger; Katsumi Higaki; Sabine Hilfiker; Bradford G Hill; Joseph A Hill; William D Hill; Keisuke Hino; Daniel Hofius; Paul Hofman; Günter U Höglinger; Jörg Höhfeld; Marina K Holz; Yonggeun Hong; David A Hood; Jeroen Jm Hoozemans; Thorsten Hoppe; Chin Hsu; Chin-Yuan Hsu; Li-Chung Hsu; Dong Hu; Guochang Hu; Hong-Ming Hu; Hongbo Hu; Ming Chang Hu; Yu-Chen Hu; Zhuo-Wei Hu; Fang Hua; Ya Hua; Canhua Huang; Huey-Lan Huang; Kuo-How Huang; Kuo-Yang Huang; Shile Huang; Shiqian Huang; Wei-Pang Huang; Yi-Ran Huang; Yong Huang; Yunfei Huang; Tobias B Huber; Patricia Huebbe; Won-Ki Huh; Juha J Hulmi; Gang Min Hur; James H Hurley; Zvenyslava Husak; Sabah Na Hussain; Salik Hussain; Jung Jin Hwang; Seungmin Hwang; Thomas Is Hwang; Atsuhiro Ichihara; Yuzuru Imai; Carol Imbriano; Megumi Inomata; Takeshi Into; Valentina Iovane; Juan L Iovanna; Renato V Iozzo; Nancy Y Ip; Javier E Irazoqui; Pablo Iribarren; Yoshitaka Isaka; Aleksandra J Isakovic; Harry Ischiropoulos; Jeffrey S Isenberg; Mohammad Ishaq; Hiroyuki Ishida; Isao Ishii; Jane E Ishmael; Ciro Isidoro; Ken-Ichi Isobe; Erika Isono; Shohreh Issazadeh-Navikas; Koji Itahana; Eisuke Itakura; Andrei I Ivanov; Anand Krishnan V Iyer; José M Izquierdo; Yotaro Izumi; Valentina Izzo; Marja Jäättelä; Nadia Jaber; Daniel John Jackson; William T Jackson; Tony George Jacob; Thomas S Jacques; Chinnaswamy Jagannath; Ashish Jain; Nihar Ranjan Jana; Byoung Kuk Jang; Alkesh Jani; Bassam Janji; Paulo Roberto Jannig; Patric J Jansson; Steve Jean; Marina Jendrach; Ju-Hong Jeon; Niels Jessen; Eui-Bae Jeung; Kailiang Jia; Lijun Jia; Hong Jiang; Hongchi Jiang; Liwen Jiang; Teng Jiang; Xiaoyan Jiang; Xuejun Jiang; Xuejun Jiang; Ying Jiang; Yongjun Jiang; Alberto Jiménez; Cheng Jin; Hongchuan Jin; Lei Jin; Meiyan Jin; Shengkan Jin; Umesh Kumar Jinwal; Eun-Kyeong Jo; Terje Johansen; Daniel E Johnson; Gail Vw Johnson; James D Johnson; Eric Jonasch; Chris Jones; Leo Ab Joosten; Joaquin Jordan; Anna-Maria Joseph; Bertrand Joseph; Annie M Joubert; Dianwen Ju; Jingfang Ju; Hsueh-Fen Juan; Katrin Juenemann; Gábor Juhász; Hye Seung Jung; Jae U Jung; Yong-Keun Jung; Heinz Jungbluth; Matthew J Justice; Barry Jutten; Nadeem O Kaakoush; Kai Kaarniranta; Allen Kaasik; Tomohiro Kabuta; Bertrand Kaeffer; Katarina Kågedal; Alon Kahana; Shingo Kajimura; Or Kakhlon; Manjula Kalia; Dhan V Kalvakolanu; Yoshiaki Kamada; Konstantinos Kambas; Vitaliy O Kaminskyy; Harm H Kampinga; Mustapha Kandouz; Chanhee Kang; Rui Kang; Tae-Cheon Kang; Tomotake Kanki; Thirumala-Devi Kanneganti; Haruo Kanno; Anumantha G Kanthasamy; Marc Kantorow; Maria Kaparakis-Liaskos; Orsolya Kapuy; Vassiliki Karantza; Md Razaul Karim; Parimal Karmakar; Arthur Kaser; Susmita Kaushik; Thomas Kawula; A Murat Kaynar; Po-Yuan Ke; Zun-Ji Ke; John H Kehrl; Kate E Keller; Jongsook Kim Kemper; Anne K Kenworthy; Oliver Kepp; Andreas Kern; Santosh Kesari; David Kessel; Robin Ketteler; Isis do Carmo Kettelhut; Bilon Khambu; Muzamil Majid Khan; Vinoth Km Khandelwal; Sangeeta Khare; Juliann G Kiang; Amy A Kiger; Akio Kihara; Arianna L Kim; Cheol Hyeon Kim; Deok Ryong Kim; Do-Hyung Kim; Eung Kweon Kim; Hye Young Kim; Hyung-Ryong Kim; Jae-Sung Kim; Jeong Hun Kim; Jin Cheon Kim; Jin Hyoung Kim; Kwang Woon Kim; Michael D Kim; Moon-Moo Kim; Peter K Kim; Seong Who Kim; Soo-Youl Kim; Yong-Sun Kim; Yonghyun Kim; Adi Kimchi; Alec C Kimmelman; Tomonori Kimura; Jason S King; Karla Kirkegaard; Vladimir Kirkin; Lorrie A Kirshenbaum; Shuji Kishi; Yasuo Kitajima; Katsuhiko Kitamoto; Yasushi Kitaoka; Kaio Kitazato; Rudolf A Kley; Walter T Klimecki; Michael Klinkenberg; Jochen Klucken; Helene Knævelsrud; Erwin Knecht; Laura Knuppertz; Jiunn-Liang Ko; Satoru Kobayashi; Jan C Koch; Christelle Koechlin-Ramonatxo; Ulrich Koenig; Young Ho Koh; Katja Köhler; Sepp D Kohlwein; Masato Koike; Masaaki Komatsu; Eiki Kominami; Dexin Kong; Hee Jeong Kong; Eumorphia G Konstantakou; Benjamin T Kopp; Tamas Korcsmaros; Laura Korhonen; Viktor I Korolchuk; Nadya V Koshkina; Yanjun Kou; Michael I Koukourakis; Constantinos Koumenis; Attila L Kovács; Tibor Kovács; Werner J Kovacs; Daisuke Koya; Claudine Kraft; Dimitri Krainc; Helmut Kramer; Tamara Kravic-Stevovic; Wilhelm Krek; Carole Kretz-Remy; Roswitha Krick; Malathi Krishnamurthy; Janos Kriston-Vizi; Guido Kroemer; Michael C Kruer; Rejko Kruger; Nicholas T Ktistakis; Kazuyuki Kuchitsu; Christian Kuhn; Addanki Pratap Kumar; Anuj Kumar; Ashok Kumar; Deepak Kumar; Dhiraj Kumar; Rakesh Kumar; Sharad Kumar; Mondira Kundu; Hsing-Jien Kung; Atsushi Kuno; Sheng-Han Kuo; Jeff Kuret; Tino Kurz; Terry Kwok; Taeg Kyu Kwon; Yong Tae Kwon; Irene Kyrmizi; Albert R La Spada; Frank Lafont; Tim Lahm; Aparna Lakkaraju; Truong Lam; Trond Lamark; Steve Lancel; Terry H Landowski; Darius J R Lane; Jon D Lane; Cinzia Lanzi; Pierre Lapaquette; Louis R Lapierre; Jocelyn Laporte; Johanna Laukkarinen; Gordon W Laurie; Sergio Lavandero; Lena Lavie; Matthew J LaVoie; Betty Yuen Kwan Law; Helen Ka-Wai Law; Kelsey B Law; Robert Layfield; Pedro A Lazo; Laurent Le Cam; Karine G Le Roch; Hervé Le Stunff; Vijittra Leardkamolkarn; Marc Lecuit; Byung-Hoon Lee; Che-Hsin Lee; Erinna F Lee; Gyun Min Lee; He-Jin Lee; Hsinyu Lee; Jae Keun Lee; Jongdae Lee; Ju-Hyun Lee; Jun Hee Lee; Michael Lee; Myung-Shik Lee; Patty J Lee; Sam W Lee; Seung-Jae Lee; Shiow-Ju Lee; Stella Y Lee; Sug Hyung Lee; Sung Sik Lee; Sung-Joon Lee; Sunhee Lee; Ying-Ray Lee; Yong J Lee; Young H Lee; Christiaan Leeuwenburgh; Sylvain Lefort; Renaud Legouis; Jinzhi Lei; Qun-Ying Lei; David A Leib; Gil Leibowitz; Istvan Lekli; Stéphane D Lemaire; John J Lemasters; Marius K Lemberg; Antoinette Lemoine; Shuilong Leng; Guido Lenz; Paola Lenzi; Lilach O Lerman; Daniele Lettieri Barbato; Julia I-Ju Leu; Hing Y Leung; Beth Levine; Patrick A Lewis; Frank Lezoualc'h; Chi Li; Faqiang Li; Feng-Jun Li; Jun Li; Ke Li; Lian Li; Min Li; Min Li; Qiang Li; Rui Li; Sheng Li; Wei Li; Wei Li; Xiaotao Li; Yumin Li; Jiqin Lian; Chengyu Liang; Qiangrong Liang; Yulin Liao; Joana Liberal; Pawel P Liberski; Pearl Lie; Andrew P Lieberman; Hyunjung Jade Lim; Kah-Leong Lim; Kyu Lim; Raquel T Lima; Chang-Shen Lin; Chiou-Feng Lin; Fang Lin; Fangming Lin; Fu-Cheng Lin; Kui Lin; Kwang-Huei Lin; Pei-Hui Lin; Tianwei Lin; Wan-Wan Lin; Yee-Shin Lin; Yong Lin; Rafael Linden; Dan Lindholm; Lisa M Lindqvist; Paul Lingor; Andreas Linkermann; Lance A Liotta; Marta M Lipinski; Vitor A Lira; Michael P Lisanti; Paloma B Liton; Bo Liu; Chong Liu; Chun-Feng Liu; Fei Liu; Hung-Jen Liu; Jianxun Liu; Jing-Jing Liu; Jing-Lan Liu; Ke Liu; Leyuan Liu; Liang Liu; Quentin Liu; Rong-Yu Liu; Shiming Liu; Shuwen Liu; Wei Liu; Xian-De Liu; Xiangguo Liu; Xiao-Hong Liu; Xinfeng Liu; Xu Liu; Xueqin Liu; Yang Liu; Yule Liu; Zexian Liu; Zhe Liu; Juan P Liuzzi; Gérard Lizard; Mila Ljujic; Irfan J Lodhi; Susan E Logue; Bal L Lokeshwar; Yun Chau Long; Sagar Lonial; Benjamin Loos; Carlos López-Otín; Cristina López-Vicario; Mar Lorente; Philip L Lorenzi; Péter Lõrincz; Marek Los; Michael T Lotze; Penny E Lovat; Binfeng Lu; Bo Lu; Jiahong Lu; Qing Lu; She-Min Lu; Shuyan Lu; Yingying Lu; Frédéric Luciano; Shirley Luckhart; John Milton Lucocq; Paula Ludovico; Aurelia Lugea; Nicholas W Lukacs; Julian J Lum; Anders H Lund; Honglin Luo; Jia Luo; Shouqing Luo; Claudio Luparello; Timothy Lyons; Jianjie Ma; Yi Ma; Yong Ma; Zhenyi Ma; Juliano Machado; Glaucia M Machado-Santelli; Fernando Macian; Gustavo C MacIntosh; Jeffrey P MacKeigan; Kay F Macleod; John D MacMicking; Lee Ann MacMillan-Crow; Frank Madeo; Muniswamy Madesh; Julio Madrigal-Matute; Akiko Maeda; Tatsuya Maeda; Gustavo Maegawa; Emilia Maellaro; Hannelore Maes; Marta Magariños; Kenneth Maiese; Tapas K Maiti; Luigi Maiuri; Maria Chiara Maiuri; Carl G Maki; Roland Malli; Walter Malorni; Alina Maloyan; Fathia Mami-Chouaib; Na Man; Joseph D Mancias; Eva-Maria Mandelkow; Michael A Mandell; Angelo A Manfredi; Serge N Manié; Claudia Manzoni; Kai Mao; Zixu Mao; Zong-Wan Mao; Philippe Marambaud; Anna Maria Marconi; Zvonimir Marelja; Gabriella Marfe; Marta Margeta; Eva Margittai; Muriel Mari; Francesca V Mariani; Concepcio Marin; Sara Marinelli; Guillermo Mariño; Ivanka Markovic; Rebecca Marquez; Alberto M Martelli; Sascha Martens; Katie R Martin; Seamus J Martin; Shaun Martin; Miguel A Martin-Acebes; Paloma Martín-Sanz; Camille Martinand-Mari; Wim Martinet; Jennifer Martinez; Nuria Martinez-Lopez; Ubaldo Martinez-Outschoorn; Moisés Martínez-Velázquez; Marta Martinez-Vicente; Waleska Kerllen Martins; Hirosato Mashima; James A Mastrianni; Giuseppe Matarese; Paola Matarrese; Roberto Mateo; Satoaki Matoba; Naomichi Matsumoto; Takehiko Matsushita; Akira Matsuura; Takeshi Matsuzawa; Mark P Mattson; Soledad Matus; Norma Maugeri; Caroline Mauvezin; Andreas Mayer; Dusica Maysinger; Guillermo D Mazzolini; Mary Kate McBrayer; Kimberly McCall; Craig McCormick; Gerald M McInerney; Skye C McIver; Sharon McKenna; John J McMahon; Iain A McNeish; Fatima Mechta-Grigoriou; Jan Paul Medema; Diego L Medina; Klara Megyeri; Maryam Mehrpour; Jawahar L Mehta; Yide Mei; Ute-Christiane Meier; Alfred J Meijer; Alicia Meléndez; Gerry Melino; Sonia Melino; Edesio Jose Tenorio de Melo; Maria A Mena; Marc D Meneghini; Javier A Menendez; Regina Menezes; Liesu Meng; Ling-Hua Meng; Songshu Meng; 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Authors: Benjamin D Varco-Merth; William Brantley; Alejandra Marenco; Derick D Duell; Devin N Fachko; Brian Richardson; Kathleen Busman-Sahay; Danica Shao; Walter Flores; Kathleen Engelman; Yoshinori Fukazawa; Scott W Wong; Rebecca L Skalsky; Jeremy Smedley; Michael K Axthelm; Jeffrey D Lifson; Jacob D Estes; Paul T Edlefsen; Louis J Picker; Cheryl Ma Cameron; Timothy J Henrich; Afam A Okoye Journal: J Clin Invest Date: 2022-05-16 Impact factor: 19.456
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