Results 21 to 30 of about 298,121 (314)
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
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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
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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]
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
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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.
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Cell death: Shadow Baxing [PDF]
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
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Unlatched BAX Pairs for Death [PDF]
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
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Apoptosis status and proliferative activity in mucopolysaccharidosis type I mice tongue mucosa cells
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
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RelA/NF-kappaB recruitment on the bax gene promoter antagonizes p73-dependent apoptosis in costimulated T cells [PDF]
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
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BAX-Dependent and BAX-Independent Regulation of Kiss1 Neuron Development in Mice [PDF]
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
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Chemical modulation of cytosolic BAX homodimer potentiates BAX activation and apoptosis
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
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