Neither loss of Bik alone, nor combined loss of Bik and Noxa, accelerate murine lymphoma development or render lymphoma cells resistant to DNA damaging drugs.

Cell Death & Disease
Lina HappoClare Scott

Abstract

The pro-apoptotic BH3-only protein, BIK, is widely expressed and although many critical functions in developmental or stress-induced death have been ascribed to this protein, mice lacking Bik display no overt abnormalities. It has been postulated that Bik can serve as a tumour suppressor, on the basis that its deficiency and loss of apoptotic function have been reported in many human cancers, including lymphoid malignancies. Evasion of apoptosis is a major factor contributing to c-Myc-induced tumour development, but despite this, we found that Bik deficiency did not accelerate Eμ-Myc-induced lymphomagenesis. Co-operation between BIK and NOXA, another BH3-only protein, has been previously described, and was attributed to their complementary binding specificities to distinct subsets of pro-survival BCL-2 family proteins. Nevertheless, combined deficiency of Bik and Noxa did not alter the onset of Eμ-Myc transgene induced lymphoma development. Moreover, although p53-mediated induction of Bik has been reported, neither Eμ-Myc/Bik(-/-) nor Eμ-Myc/Bik(-/-)Noxa(-/-) lymphomas were more resistant than control Eμ-Myc lymphomas to killing by DNA damaging drugs, either in vitro or in vivo. These results suggest that Bik, even in combinati...Continue Reading

References

Oct 8, 1992·Nature·R P BissonnetteD R Green
Jan 1, 1994·Current Biology : CB·T JacksR A Weinberg
May 9, 1998·The Journal of Biological Chemistry·R HegdeE S Alnemri
Oct 29, 1999·Genes & Development·C M EischenJ L Cleveland
Oct 5, 2001·Nature Reviews. Molecular Cell Biology·C J Sherr
Mar 9, 2002·The Journal of Biological Chemistry·Marc GermainGordon C Shore
Jun 28, 2002·Cancer Cell·Clemens A SchmittScott W Lowe
Apr 14, 2004·Proceedings of the National Academy of Sciences of the United States of America·Alexander EgleSuzanne Cory
Oct 27, 2004·Apoptosis : an International Journal on Programmed Cell Death·C PaquetR Bertrand
Oct 10, 2006·FEBS Letters·Pedro J RealJose L Fernandez-Luna
Feb 27, 2007·Oncogene·J M Adams, S Cory
Mar 4, 2008·Trends in Cell Biology·Jerry E Chipuk, Douglas R Green
Jun 25, 2008·Molecular and Cellular Biology·Sean P GarrisonGerard P Zambetti
Sep 2, 2008·Oncogene·G P Dotto
Jan 17, 2009·Cell Death and Differentiation·E M MichalakC L Scott
Jun 12, 2010·Blood·Andreas Beilhack

❮ Previous
Next ❯

Citations

May 13, 2008·The Journal of Pain : Official Journal of the American Pain Society·Reza RastmaneshCharles Edwards Weber
Mar 25, 2014·Oncotarget·Ivana CelardoGerry Melino
Jan 24, 2019·Frontiers in Oncology·Clare M AdamsChristine M Eischen

❮ Previous
Next ❯

Methods Mentioned

BETA
PCR
transgenic
flow cytometry

Software Mentioned

Prism
Stata
GraphPad
R
GraphPad Prism

Related Concepts

Related Feeds

BCL-2 Family Proteins

BLC-2 family proteins are a group that share the same homologous BH domain. They play many different roles including pro-survival signals, mitochondria-mediated apoptosis and removal or damaged cells. They are often regulated by phosphorylation, affecting their catalytic activity. Here is the latest research on BCL-2 family proteins.

Apoptosis in Cancer

Apoptosis is an important mechanism in cancer. By evading apoptosis, tumors can continue to grow without regulation and metastasize systemically. Many therapies are evaluating the use of pro-apoptotic activation to eliminate cancer growth. Here is the latest research on apoptosis in cancer.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis