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Keywords: Bcl-2
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Journal Articles
J Cell Sci (2020) 133 (12): jcs241034.
Published: 24 June 2020
... inhibiting the activation of JNK and autophagic signaling following nutrient starvation. The precise molecular mechanisms linking Gαi3 to both stress and growth factor signaling remain poorly understood. Importantly, JNK-mediated phosphorylation of Bcl-2 was previously found to activate autophagic signaling...
Includes: Supplementary data
Journal Articles
J Cell Sci (2014) 127 (12): 2782–2792.
Published: 15 June 2014
...Tim Vervliet; Elke Decrock; Jordi Molgó; Vincenzo Sorrentino; Ludwig Missiaen; Luc Leybaert; Humbert De Smedt; Nael Nadif Kasri; Jan B. Parys; Geert Bultynck ABSTRACT The anti-apoptotic B-cell lymphoma-2 (Bcl-2) protein not only counteracts apoptosis at the mitochondria by scaffolding pro-apoptotic...
Includes: Supplementary data
Journal Articles
J Cell Sci (2012) 125 (21): 5233–5240.
Published: 01 November 2012
... inhibitory factor Ras suppressor protein-1 (RSU-1), whose stability was severely reduced upon loss of PINCH-1. Chemical inhibition of JNK attenuated apoptosis of PrE cells but failed to reduce Bax activity. The increased Bax activity was associated with reduced integrin signalling and diminished Bcl-2 levels...
Includes: Supplementary data
Journal Articles
J Cell Sci (2008) 121 (20): 3373–3382.
Published: 15 October 2008
... Biologists Limited 2008 2008 Bcl-2 BCL2 CED-9 DRP-1 Mitochondria Morphology Dynamics Homeostasis C. elegans Transmembrane domain Bcl-2 proteins regulate apoptosis through a mechanism that is sensitive to their expression levels, which vary among Bcl-2 homologs and different tumor...
Includes: Supplementary data
Journal Articles
J Cell Sci (2007) 120 (3): 379–383.
Published: 01 February 2007
... AKT mTOR BCL-2 Beclin1 Cancer Cancer is a disease in which inherent genetic flexibility allows cells to progressively evolve functions that promote cell growth, disable cell death mechanisms and evade immune surveillance and therapy ( Hanahan and Weinberg, 2000 ). Regulation of cell growth...
Journal Articles
J Cell Sci (2005) 118 (14): 3091–3102.
Published: 15 July 2005
... transmembrane potential, caspase activation and chromatin condensation. While caspase inhibition retarded cell death, it had no protective effect on mitochondria. Stabilization of mitochondria by overexpression of Bcl-2 or the mitochondrion-targeted cytomegalovirus protein vMIA, however, blocked all signs of...
Journal Articles
J Cell Sci (2005) 118 (5): 863–872.
Published: 01 March 2005
... developmental events: the loss of Bcl-2 expression by neurons and the maturation of astrocytes. Before postnatal day 4, when astrocytes are immature, overexpression of Bcl-2 alone supported robust and rapid optic nerve regeneration over long distances, leading to innervation of brain targets by day 4 in mice...
Journal Articles
J Cell Sci (2005) 118 (3): 473–483.
Published: 01 February 2005
... of mitochondria is still unclear, the activation of multidomain pro-apoptotic proteins of the Bcl-2 family, such as Bax and Bak, is evidently crucial. Regulation of Bax and Bak by other members of the family has been known for a long time, but recent evidence suggests that additional unrelated...
Journal Articles
J Cell Sci (2004) 117 (23): 5643–5653.
Published: 01 November 2004
... contain a nucleus or mitochondrial DNA, yet was inhibited when two mitochondrion-stabilizing proteins, Bcl-2 or vMIA, were overexpressed. Contagious apoptosis could be induced in primary human T cells, as well as in vivo, in T cells exposed to dying Env-expressing cells. Altogether, these data point to a...
Journal Articles
J Cell Sci (2004) 117 (13): 2641–2651.
Published: 01 June 2004
...-mediated pathways to apoptosis. Hsps can inhibit the activity of pro-apoptotic Bcl-2 proteins to prevent permeabilization of the outer mitochondrial membrane and release of apoptogenic factors. The disruption of apoptosome formation represents another mechanism by which Hsps can prevent caspase activation...
Journal Articles
J Cell Sci (2003) 116 (22): 4493–4499.
Published: 15 November 2003
...Michael J. Thomenius; Clark W. Distelhorst Bcl-2 has been described both as an inhibitor of programmed cell death and as an inhibitor of mitochondrial dysfunction during apoptosis. It is still not clear what biochemical activity of Bcl-2 is responsible for its function, but increasing evidence...
Journal Articles
J Cell Sci (2003) 116 (18): 3687–3700.
Published: 15 September 2003
...Laiji Li; Jody Backer; Annisa S. K. Wong; Erin L. Schwanke; Brian G. Stewart; Manijeh Pasdar Bcl-2, a member of the apoptosis-regulating family of proteins confers a survival advantage on cells by inhibiting apoptosis. Bcl-2 expression is estrogen-responsive and high in various tumors...
Journal Articles
J Cell Sci (2002) 115 (8): 1567–1574.
Published: 15 April 2002
...Philippe Bouillet; Andreas Strasser The BH3-only members of the Bcl-2 protein family are essential initiators of programmed cell death and are required for apoptosis induced by cytotoxic stimuli. These proteins have evolved to recognise distinct forms of cell stress. In response, they unleash the...
Journal Articles
J Cell Sci (2001) 114 (23): 4161–4172.
Published: 01 December 2001
...Justine Rudner; Albrecht Lepple-Wienhues; Wilfried Budach; Johannes Berschauer; Björn Friedrich; Sebastian Wesselborg; Klaus Schulze-Osthoff; Claus Belka The proto-oncogene Bcl-2 is expressed in membranes of mitochondria and endoplasmic reticulum and mediates resistance against a broad range of...