Literature DB >> 11423909

Tissue expression and subcellular localization of the pro-survival molecule Bcl-w.

L A O'Reilly1, C Print, G Hausmann, K Moriishi, S Cory, D C Huang, A Strasser.   

Abstract

Anti-apoptotic members of the Bcl-2 family, such as Bcl-w, maintain cell viability by preventing the activation of the cell death effectors, the caspases. Gene targeting experiments in mice have demonstrated that Bcl-w is required for spermatogenesis and for survival of damaged epithelial cells in the gut. Bcl-w is, however, dispensable for physiological cell death in other tissues. Here we report on the analysis of Bcl-w protein expression using a panel of novel monoclonal antibodies. Bcl-w is found in a diverse range of tissues including colon, brain and testes. A survey of transformed cell lines and purified hematopoietic cells demonstrated that Bcl-w is expressed in cells of myeloid, lymphoid and epithelial origin. Subcellular fractionation and confocal laser scanning microscopy demonstrated that Bcl-w protein is associated with intracellular membranes. The implications of these results are discussed in the context of the phenotype of Bcl-w-null mice and recent data that suggest that Bcl-w may play a role in colon carcinogenesis.

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Year:  2001        PMID: 11423909     DOI: 10.1038/sj.cdd.4400835

Source DB:  PubMed          Journal:  Cell Death Differ        ISSN: 1350-9047            Impact factor:   15.828


  35 in total

1.  The structure of Bcl-w reveals a role for the C-terminal residues in modulating biological activity.

Authors:  Mark G Hinds; Martin Lackmann; Gretchen L Skea; Penny J Harrison; David C S Huang; Catherine L Day
Journal:  EMBO J       Date:  2003-04-01       Impact factor: 11.598

2.  The antiapoptotic protein Mcl-1 controls the type of cell death in Theiler's virus-infected BHK-21 cells.

Authors:  Sevim Yildiz Arslan; Kyung-No Son; Howard L Lipton
Journal:  J Virol       Date:  2011-11-30       Impact factor: 5.103

3.  Sensory neuropathy attributable to loss of Bcl-w.

Authors:  Stephanie L Courchesne; Christoph Karch; Maria F Pazyra-Murphy; Rosalind A Segal
Journal:  J Neurosci       Date:  2011-02-02       Impact factor: 6.167

4.  Prophylactic treatment with the BH3 mimetic ABT-737 impedes Myc-driven lymphomagenesis in mice.

Authors:  P N Kelly; S Grabow; A R D Delbridge; J M Adams; A Strasser
Journal:  Cell Death Differ       Date:  2012-07-20       Impact factor: 15.828

Review 5.  The essential role of evasion from cell death in cancer.

Authors:  Gemma L Kelly; Andreas Strasser
Journal:  Adv Cancer Res       Date:  2011       Impact factor: 6.242

6.  Both leukaemic and normal peripheral B lymphoid cells are highly sensitive to the selective pharmacological inhibition of prosurvival Bcl-2 with ABT-199.

Authors:  S L Khaw; D Mérino; M A Anderson; S P Glaser; P Bouillet; A W Roberts; D C S Huang
Journal:  Leukemia       Date:  2014-01-09       Impact factor: 11.528

7.  BCL-W has a fundamental role in B cell survival and lymphomagenesis.

Authors:  Clare M Adams; Annette S Kim; Ramkrishna Mitra; John K Choi; Jerald Z Gong; Christine M Eischen
Journal:  J Clin Invest       Date:  2017-01-17       Impact factor: 14.808

8.  Non-Hodgkin and Hodgkin Lymphomas Select for Overexpression of BCLW.

Authors:  Clare M Adams; Ramkrishna Mitra; Jerald Z Gong; Christine M Eischen
Journal:  Clin Cancer Res       Date:  2017-08-29       Impact factor: 12.531

9.  Bcl-x(L) sequesters its C-terminal membrane anchor in soluble, cytosolic homodimers.

Authors:  Seon-Yong Jeong; Brigitte Gaume; Yang-Ja Lee; Yi-Te Hsu; Seung-Wook Ryu; Soo-Han Yoon; Richard J Youle
Journal:  EMBO J       Date:  2004-05-06       Impact factor: 11.598

10.  Co-inhibition of BCL-W and BCL2 restores antiestrogen sensitivity through BECN1 and promotes an autophagy-associated necrosis.

Authors:  Anatasha C Crawford; Rebecca B Riggins; Ayesha N Shajahan; Alan Zwart; Robert Clarke
Journal:  PLoS One       Date:  2010-01-06       Impact factor: 3.240

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