Literature DB >> 25642943

Correction: The tumor suppressor gene, RASSF1A, is essential for protection against inflammation -induced injury.

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Abstract

[This corrects the article DOI: 10.1371/journal.pone.0075483.].

Entities:  

Year:  2015        PMID: 25642943      PMCID: PMC4313949          DOI: 10.1371/journal.pone.0118034

Source DB:  PubMed          Journal:  PLoS One        ISSN: 1932-6203            Impact factor:   3.240


There is an error in the legend for Fig. 8. Please see the corrected Fig. 8 here.
Figure 8

The PTK inhibitor, imatinib, inhibits the appearance of pY-YAP and promoted increased survival of Rassf1a but not Rassf1a mice animals following inflammation-induced injury.

(A) Rassf1a or Rassf1a mice were intraperitoneally injected with the PTK inhibitor, imatinib at 60 mg/kg body weight on days 3 and 6 following 3% DSS addition. P-value between survival of DSS-treated wild type and Rassf1a was <0.0001 (n = 17) and between DSS-treated Rassf1a (+ imatinib) versus DSS-treated Rassf1a was 0.0086 (n = 17). No significance difference was observed between DSS-treated Rassf1a and DSS-treated Rassf1a (+ imatinib) mice (please see Fig. 1A for the survival curve of DSS-treated Rassf1a mice). Following DSS/gleevec treatment, (B) histological analysis of colonic sections, (C) serum IL-6, (D) cell death via PARP (late marker of apoptosis); (E) phospho-YAP by IHC, and (F) In vitro kinase activity was carried out for c-Abl using colon lystes from DSS-treated wild type and Rassf1a (top panel) and Rassf1a (bottom panel) mice with overexpressed FLAG-YAP as substrate. Expression levels of c-Abl were similar in all the lanes (data not shown) and bacterially expressed GST or GST-1A (1A) was used to explore how RASSF1A may directly interfere with c-Abl kinase activity. Expression of FLAG-YAP, GST and GST-1A are shown in Fig. S7D. For (B) p-value between wild type versus Rassf1a mice (+DSS) was 0.004, wild type versus Rassf1a mice + DSS + gleevec) was 0.168 and wild type versus Rassf1a mice (+DSS + gleevec) was 0.452 (n = 4 – 8). For (C), p-value between wild type versus Rassf1a mice (+DSS) was 0.004 and wild type versus Rassf1a mice (+ DSS + gleevec) was 0.347 and wild type versusRassf1a mice (+DSS + gleevec) was 0.262 (n = 4 – 8). For (E) P values of Rassf1a mice orRassf1a mice (+DSS −/+ gleevec) was <0.001 (n = 10).

The PTK inhibitor, imatinib, inhibits the appearance of pY-YAP and promoted increased survival of Rassf1a but not Rassf1a mice animals following inflammation-induced injury.

(A) Rassf1a or Rassf1a mice were intraperitoneally injected with the PTK inhibitor, imatinib at 60 mg/kg body weight on days 3 and 6 following 3% DSS addition. P-value between survival of DSS-treated wild type and Rassf1a was <0.0001 (n = 17) and between DSS-treated Rassf1a (+ imatinib) versus DSS-treated Rassf1a was 0.0086 (n = 17). No significance difference was observed between DSS-treated Rassf1a and DSS-treated Rassf1a (+ imatinib) mice (please see Fig. 1A for the survival curve of DSS-treated Rassf1a mice). Following DSS/gleevec treatment, (B) histological analysis of colonic sections, (C) serum IL-6, (D) cell death via PARP (late marker of apoptosis); (E) phospho-YAP by IHC, and (F) In vitro kinase activity was carried out for c-Abl using colon lystes from DSS-treated wild type and Rassf1a (top panel) and Rassf1a (bottom panel) mice with overexpressed FLAG-YAP as substrate. Expression levels of c-Abl were similar in all the lanes (data not shown) and bacterially expressed GST or GST-1A (1A) was used to explore how RASSF1A may directly interfere with c-Abl kinase activity. Expression of FLAG-YAP, GST and GST-1A are shown in Fig. S7D. For (B) p-value between wild type versus Rassf1a mice (+DSS) was 0.004, wild type versus Rassf1a mice + DSS + gleevec) was 0.168 and wild type versus Rassf1a mice (+DSS + gleevec) was 0.452 (n = 4 – 8). For (C), p-value between wild type versus Rassf1a mice (+DSS) was 0.004 and wild type versus Rassf1a mice (+ DSS + gleevec) was 0.347 and wild type versusRassf1a mice (+DSS + gleevec) was 0.262 (n = 4 – 8). For (E) P values of Rassf1a mice orRassf1a mice (+DSS −/+ gleevec) was <0.001 (n = 10).
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1.  The tumor suppressor gene, RASSF1A, is essential for protection against inflammation -induced injury.

Authors:  Marilyn Gordon; Mohamed El-Kalla; Yuewen Zhao; Yahya Fiteih; Jennifer Law; Natalia Volodko; Anwar Anwar-Mohamed; Anwar Mohamed; Ayman O S El-Kadi; Lei Liu; Jeff Odenbach; Aducio Thiesen; Christina Onyskiw; Haya Abu Ghazaleh; Jikyoung Park; Sean Bong Lee; Victor C Yu; Carlos Fernandez-Patron; R Todd Alexander; Eytan Wine; Shairaz Baksh
Journal:  PLoS One       Date:  2013-10-16       Impact factor: 3.240

  1 in total

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