Literature DB >> 8632670

Expression of Id2 and Id3 mRNA in human lymphocytes.

A Ishiguro1, K Spirin, M Shiohara, A Tobler, J D Norton, M Rigolet, T Shimbo, H P Koeffler.   

Abstract

Helix-loop-helix (HLH) transcription factors are involved in cellular growth and differentiation. The Id (inhibitor of DNA binding and differentiation) HLH proteins, in a dominantly negative fashion, regulate transcriptional activities of basic HLH proteins. We examined by northern hybridization the expression of Id2 and Id3 mRNA in human leukemia/lymphoma lines and patient samples, as well as resting and activated normal human lymphocytes from peripheral blood (PBL). The Id2 mRNA was abundantly expressed in 5/12 T-cell and 3/4 B-cell lines, and Id3 mRNA was detected in 4/12 T-cell and 3/4 B-cell lines. Interestingly, Id2, but not Id3, mRNA was strongly expressed in 4/5 T-cell lines infected with human T-cell leukemia virus type I (HTLV-I) (ATL-1k, MT-2, S-LB1) and type II (Mo). Another unexpected finding was that T-cell leukemias and T-cell lines often expressed either Id2 or Id3 mRNA. In addition, resting PBL constitutively expressed prominent levels of Id2 mRNA, but not Id3 mRNA. Upon PHA-stimulation, Id2 expression decreased and Id3 levels increased with biphasic kinetics. Taken together, our studies revealed three unexpected findings which require further analysis: (1) expression of Id2 mRNA is often associated with lymphocytic transformation by HTLV-I or -II; (2) T-cells usually express either Id2 or Id3 mRNA, but B-cells often express both simultaneously; (3) non-dividing, normal PBL express high levels of Id2 and no Id3 mRNA; and with the onset of cellular proliferation, levels of Id2 mRNA decrease while levels of Id3 mRNA increase, suggesting that regulation of expression of these closely related genes is disparate.

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Year:  1995        PMID: 8632670     DOI: 10.1016/0145-2126(95)00084-4

Source DB:  PubMed          Journal:  Leuk Res        ISSN: 0145-2126            Impact factor:   3.156


  7 in total

1.  Structure of a dominant-negative helix-loop-helix transcriptional regulator suggests mechanisms of autoinhibition.

Authors:  Ryohei Ishii; Kazunobu Isogaya; Azusa Seto; Daizo Koinuma; Yuji Watanabe; Fumio Arisaka; So-ichi Yaguchi; Hiroaki Ikushima; Naoshi Dohmae; Kohei Miyazono; Keiji Miyazawa; Ryuichiro Ishitani; Osamu Nureki
Journal:  EMBO J       Date:  2012-03-27       Impact factor: 11.598

2.  Id2 promotes apoptosis by a novel mechanism independent of dimerization to basic helix-loop-helix factors.

Authors:  M Florio; M C Hernandez; H Yang; H K Shu; J L Cleveland; M A Israel
Journal:  Mol Cell Biol       Date:  1998-09       Impact factor: 4.272

3.  Sequestration of E12/E47 and suppression of p27KIP1 play a role in Id2-induced proliferation and tumorigenesis.

Authors:  Valerie A Trabosh; Kyle A Divito; Baltazar D Aguda; Cynthia M Simbulan-Rosenthal; Dean S Rosenthal
Journal:  Carcinogenesis       Date:  2009-05-18       Impact factor: 4.944

4.  Ectopic expression of C/EBPalpha and ID1 is sufficient to restore defective neutrophil development in low-risk myelodysplasia.

Authors:  Christian R Geest; Miranda Buitenhuis; Edo Vellenga; Paul J Coffer
Journal:  Haematologica       Date:  2009-08       Impact factor: 9.941

5.  Id1 immortalizes hematopoietic progenitors in vitro and promotes a myeloproliferative disease in vivo.

Authors:  H C Suh; W Leeanansaksiri; M Ji; K D Klarmann; K Renn; J Gooya; D Smith; I McNiece; S Lugthart; P J M Valk; R Delwel; J R Keller
Journal:  Oncogene       Date:  2008-06-09       Impact factor: 9.867

6.  Increased expression of Id1 and Id3 promotes tumorigenicity by enhancing angiogenesis and suppressing apoptosis in small cell lung cancer.

Authors:  Danqing Chen; Shiva S Forootan; John R Gosney; Farzad S Forootan; Youqiang Ke
Journal:  Genes Cancer       Date:  2014-05

Review 7.  Burrowing through the Heterogeneity: Review of Mouse Models of PTCL-NOS.

Authors:  Christine E Cutucache; Tyler A Herek
Journal:  Front Oncol       Date:  2016-09-26       Impact factor: 6.244

  7 in total

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