In cells, Bcl-rambo is localized to the mitochondria, and its overexpression induces apoptosis that is blocked by caspase inhibitors, whereas inhibitors controlling upstream events of either the 'death receptor' (FLIP, FADD-DN) or the 'mitochondrial' pro-apoptotic pathway (Bcl-x(L)) had no effect. (wikipedia.org)
Bcl-rambo mediates apoptosis by associating with adenine nucleotide translocator (ANT), a component of the mitochondrial permeability transition pore, to induce its opening. (wikipedia.org)
Autophagy1
These findings have broad implications for our understanding of 14-3-3ε function, provide an explanation for the mechanism of nucleo-cytoplasmic shuttling of hnRNP C and provide new insights into the complex regulation of autophagy. (bvsalud.org)
Stop codon2
An alternatively-spliced protein variant, called Bcl-rambo beta, is composed of only the BH4 domain, completely lacking the BH domains 1 through 3 due to an in-frame stop codon inserted by an Alu element. (wikipedia.org)
DUX4 protein sequences beginning at the ATG start codon, with the stop codon indicated, and the 3′UTRs shown in orange. (comprehensivephysiology.com)
Cell Death1
However, the form of cell death induced by 14-3-3ε translocation and mechanisms underlying this effect remain unclear. (bvsalud.org)
Protein4
Upon cytosolic entry, it serves as a cofactor in the formation of the "apoptosome," a complex consisting of the adaptor protein Apaf-1 and procaspase-9, which in turn causes the activation of caspase-9 and downstream caspases, such as caspase-3 ( Chinnaiyan, 1999 ). (rupress.org)
Translocation of 14-3-3 protein epsilon (14-3-3ε) was found to be involved in Triptolide (Tp)-induced inhibition of colorectal cancer (CRC) cell proliferation. (bvsalud.org)
AIM AND STUDY: This study aims to investigate the antifibrotic mechanism of FZHY treatment by exploring its effects on the activation of NOD-like receptor protein 3 (NLRP3) inflammasome in macrophages. (bvsalud.org)
The two DUX4‐fl isoforms produce the same protein sequence and differ only in the splicing of the 3′UTR. (comprehensivephysiology.com)
Activation1
To study inflammasome function, Lipopolysaccharide (LPS)/adenine triphosphate (ATP) induced NLRP3 inflammasome activation was induced in bone marrow-derived macrophages (BMDMs) isolated from wild mice. (bvsalud.org)
Protein1
An alternatively-spliced protein variant, called Bcl-rambo beta, is composed of only the BH4 domain, completely lacking the BH domains 1 through 3 due to an in-frame stop codon inserted by an Alu element. (wikipedia.org)
Human1
Description: A competitive ELISA for quantitative measurement of Human Mothers against decapentaplegic homolog 3(SMAD3) in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. (antibody-tech.com)
Potentially1
3. Fucosyltransferase-4 and Oligosaccharide Lewis Y Antigen as potentially Correlative Biomarkers of Helicobacter pylori CagA Associated Gastric Cancer. (nih.gov)
Domain2
The DH domain has been deduced to be responsible for guanine nucleotide exchange in CDC42 to activate downstream factors. (hiv-pharmacogenomics.org)
Our aim was to build a prokaryotic expression system for the DH domain and to examine its guanine nucleotide exchange activity toward CDC42 in vitro. (hiv-pharmacogenomics.org)
Cells4
In cells, Bcl-rambo is localized to the mitochondria, and its overexpression induces apoptosis that is blocked by caspase inhibitors, whereas inhibitors controlling upstream events of either the 'death receptor' (FLIP, FADD-DN) or the 'mitochondrial' pro-apoptotic pathway (Bcl-x(L)) had no effect. (wikipedia.org)
3BP (3 Bromo Pyruvate) is a small non-toxic molecule that induces apoptosis in cancer cells while sparing normal cells, thus providing the most promising cancer treatment we have seen in many years. (greenmedinfo.com)
6. Celecoxib inhibits Helicobacter pylori-induced invasion of gastric cancer cells through an adenine nucleotide translocator-dependent mechanism. (nih.gov)
12. Antitumor effects of celecoxib on K562 leukemia cells are mediated by cell-cycle arrest, caspase-3 activation, and downregulation of Cox-2 expression and are synergistic with hydroxyurea or imatinib. (nih.gov)