Results 11 to 20 of about 377,868 (302)

Alpha-helical destabilization of the Bcl-2-BH4-domain peptide abolishes its ability to inhibit the IP3 receptor. [PDF]

open access: yesPLoS ONE, 2013
The anti-apoptotic Bcl-2 protein is the founding member and namesake of the Bcl-2-protein family. It has recently been demonstrated that Bcl-2, apart from its anti-apoptotic role at mitochondrial membranes, can also directly interact with the inositol 1 ...
Giovanni Monaco   +12 more
doaj   +10 more sources

Small inhibitor of Bcl-2, HA14-1, selectively enhanced the apoptotic effect of cisplatin by modulating Bcl-2 family members in MDA-MB-231 breast cancer cells [PDF]

open access: yes, 2010
Inhibition or downregulation of Bcl-2 represents a new therapeutic approach to by-pass chemoresistance in cancer cells. Therefore, we explored the potential of this approach in breast cancer cells.
A Letai   +34 more
core   +1 more source

Targeting BCL-2 regulated apoptosis in cancer [PDF]

open access: yes, 2018
The ability of a cell to undergo mitochondrial apoptosis is governed by pro- and anti-apoptotic members of the BCL-2 protein family. The equilibrium of pro- versus anti-apoptotic BCL-2 proteins ensures appropriate regulation of programmed cell death ...
Campbell, Kirsteen J.   +1 more
core   +1 more source

Small molecule and peptide inhibitors of the pro-survival protein Mcl-1 [PDF]

open access: yes, 2016
The ability of protein–protein interactions to regulate cellular processes in both beneficial and detrimental ways has made them obvious drug targets.
Beekman, Andrew, Howell, Lesley
core   +1 more source

Impact of L-carnitine and selenium treatment on testicular apoptosis in rats exposed to 2.45 GHz microwave energy [PDF]

open access: yes, 2015
Objective: It has been suggested that electromagnetic radiation (EMR) by wireless devices (2.45 GHz) induces testicular apoptosis. We investigated if supplemental selenium (Se) and L-carnitine may reduce this adverse effect.
Comlekci, S.   +5 more
core   +1 more source

Bcl-2 Family Proteins [PDF]

open access: yesOncogene, 1998
Bcl-2 family proteins serve as critical regulators of pathways involved in apoptosis, acting to either inhibit or promote cell death. Altered expression of these proteins occurs commonly in human cancers, contributing to neoplastic cell expansion by suppressing programmed cell death and extending tumor cell life span. Moreover, because chemotherapeutic
openaire   +2 more sources

Predisposition to Apoptosis in Hepatocellular Carcinoma: From Mechanistic Insights to Therapeutic Strategies

open access: yesFrontiers in Oncology, 2019
Hepatocellular carcinoma (HCC) ranks among the most rapidly evolving cancers in the Western world. The majority of HCCs develop on the basis of a chronic inflammatory liver damage that predisposes liver cancer development and leads to deregulation of ...
Jens U. Marquardt   +3 more
doaj   +1 more source

Main Pro-Apoptotic Member of BCL-2 Family Proteins-BAX [PDF]

open access: yes, 2010
Programmed cell death (apoptosis) plays a vital role in the regulation of cellular homeostasis. Because of apoptosis fundamental importance, this process is highly regulated.
Kiliańska, Zofia, Żolnierczyk, Jolanta
core   +2 more sources

Guarding the Bcl-2 Army [PDF]

open access: yesCancer Biology & Therapy, 2004
Commentary to: Expression of Inducible Bcl-XS in Myeloid Leukemia: Compensatory Upregulation of Bcl-XL and Bcl-2 Prevents Apoptosis and Chemosensitization Frank Tacke, Frank C. Marini, III, Shourong Zhao, Teresa McQueen, Marina Konopleva, Peter P.
Jan, Schmidt-Mende, Boris, Zhivotovsky
openaire   +2 more sources

Ryanodine receptors are targeted by anti-apoptotic Bcl-X-L involving its BH4 domain and Lys87 from its BH3 domain [PDF]

open access: yes, 2015
Anti-apoptotic B-cell lymphoma 2 (Bcl-2) family members target several intracellular Ca2+-transport systems. Bcl-2, via its N-terminal Bcl-2 homology (BH) 4 domain, inhibits both inositol 1,4,5-trisphosphate receptors (IP(3)Rs) and ryanodine receptors ...
Bultynck, Geert   +14 more
core   +1 more source

Home - About - Disclaimer - Privacy