Results 21 to 30 of about 298,121 (314)

Bax activation by Bim? [PDF]

open access: yesCell Death & Differentiation, 2009
The mechanism by which the cell death mediator Bax becomes activated to cause mitochondrial damage, a key step for the intrinsic pathway to apoptosis, remain highly contentious. Although some data support a role for certain BH3-only proteins, such as Bim or tBid, to directly activate Bax, others have led to the conclusion that BH3-only proteins act ...
Peter E. Czabotar   +2 more
openaire   +3 more sources

The influence of BCL2, BAX, and ABCB1 gene expression on prognosis of adult de novo acute myeloid leukemia with normal karyotype patients

open access: yesRadiology and Oncology, 2023
Deregulation of the apoptotic process underlies the pathogenesis of many cancers, including leukemia, but is also very important for the success of chemotherapy treatment.
Pravdic Zlatko   +6 more
doaj   +1 more source

Distinct promoter elements mediate the co-operative effect of Brn-3a and p53 on the p21 promoter and their antagonism on the Bax promoter [PDF]

open access: yes, 2002
Although the promoters of both the Bax and p21 genes are activated by p53, they differ in the effect on this activation of the POU family transcription factor Brn-3a. Thus, Brn-3a inhibits activation of the Bax promoter by p53 but enhances the ability of
Budhram-Mahadeo, VS   +2 more
core   +2 more sources

Puma strikes Bax [PDF]

open access: yesJournal of Cell Biology, 2009
The commitment to programmed cell death via apoptosis is largely made upon activation of the proapoptotic mitochondrial proteins Bax or Bak. In this issue, Gallenne et al. (Gallenne, C., F. Gautier, L. Oliver, E. Hervouet, B. Noël, J.A. Hickman, O. Geneste, P.-F. Cartron, F.M. Vallette, S. Manon, and P. Juin. 2009. J. Cell Biol.
openaire   +2 more sources

Cell death: Shadow Baxing [PDF]

open access: yesCurrent Biology, 1998
Bcl-2, one of a family of key regulators of apoptosis, was the first cell-death machinery component to be identified, but how the family functions is still not clear. Mammalian Bax, a pro-apoptotic family member, can cause yeast cells to die, and two recent yeast genetic screens shed light on how Bax might function.
John Silke, David L. Vaux
openaire   +3 more sources

Unlatched BAX Pairs for Death [PDF]

open access: yesCell, 2013
Self-interacting BAX proteins permeabilize outer mitochondrial membranes to trigger apoptotic cell death. Czabotar et al. present two revealing structures of BAX dimers: one dimer has an activator BH3 helix bound into its canonical cleft, and the other dimer exposes a planar hydrophobic face potentially critical for membrane interactions.
J. Marie Hardwick, Heather M. Lamb
openaire   +3 more sources

Apoptosis status and proliferative activity in mucopolysaccharidosis type I mice tongue mucosa cells

open access: yesDental Research Journal, 2012
Background: Mucopolysaccharidosis type I (MPS I) is caused by a deficiency of alfa-iduronidase (IDUA), which leads to intralysosomal accumulation of glysosaminoglycans.
Juliana Noguti   +5 more
doaj   +1 more source

RelA/NF-kappaB recruitment on the bax gene promoter antagonizes p73-dependent apoptosis in costimulated T cells [PDF]

open access: yes, 2008
The balance between antiapoptotic and proapoptotic proteins of the Bcl-2 family is critical in determining the fate of T cells in response to death stimuli.
A., Annibaldi   +7 more
core   +1 more source

BAX-Dependent and BAX-Independent Regulation of Kiss1 Neuron Development in Mice [PDF]

open access: yesEndocrinology, 2010
The Kiss1 gene and its product kisspeptin are important regulators of reproduction. In rodents, Kiss1 is expressed in the hypothalamic arcuate (ARC) and anteroventral periventricular (AVPV)/rostral periventricular (PeN) nuclei. In the AVPV/PeN, females have more Kiss1 and tyrosine hydroxylase (TH) neurons than males.
Matthew C. Poling   +5 more
openaire   +3 more sources

Chemical modulation of cytosolic BAX homodimer potentiates BAX activation and apoptosis

open access: yesNature Communications, 2023
AbstractThe BCL-2 family protein BAX is a major regulator of physiological and pathological cell death. BAX predominantly resides in the cytosol in a quiescent state and upon stress, it undergoes conformational activation and mitochondrial translocation leading to mitochondrial outer membrane permeabilization, a critical event in apoptosis execution ...
Nadege Gitego   +5 more
openaire   +3 more sources

Home - About - Disclaimer - Privacy