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p53 (show TP53 ELISA Kits) and Bax (show BAX ELISA Kits) might play an important role in microcystin-LR (MC-LR)-induced apoptosis in HepG2 cells in which PUMA and survivin (show BIRC5 ELISA Kits) were involved.
Therapeutic response to non-genotoxic activation of p53 (show TP53 ELISA Kits) by Nutlin3a is driven by PUMA-mediated apoptosis in lymphoma cells.
p53 (show TP53 ELISA Kits)/PUMA expression in human pulmonary fibroblasts mediates cell activation and migration in silicosis
Suggest that the accumulation of PUMA in the cytosol may be important for the participation of this protein in apoptosis without the need for prior transcription in Burkitt's lymphoma b cells.
in vitro OGT (show OGT ELISA Kits) knockdown induced more cell apoptosis through increasing PUMA and caspase-3 (show CASP3 ELISA Kits) expression
our data purport that p53 (show TP53 ELISA Kits) not only increased Puma expression directly, but that it may also do so through miR (show MLXIP ELISA Kits)-203. Additionally, functional studies revealed that miR (show MLXIP ELISA Kits)-203 overexpression induced apoptosis and inhibited cell invasiveness.
the selective degradation of BBC3 underlies the prosurvival role of chaperone-mediated autophagy.
puma-mediated apoptosis is not induced in mucosal melanomas by cisplatin
There-fore, stable transfection of PUMA can significantly enhance epirubicin-induced apoptosis sensitivity of MCF-7 breast cancer cells.
inhibition of AKT (show AKT1 ELISA Kits)/FoxO3a (show FOXO3 ELISA Kits) signaling may contribute to H1-mediated PUMA induction, suggesting that inhibition of AKT (show AKT1 ELISA Kits)/FoxO3a (show FOXO3 ELISA Kits) signaling result in PUMA expression in response to p53 (show TP53 ELISA Kits)-independent cytotoxic effects of H1.
PUMA is dispensable for glucose homeostasis in lean and obese mice, but it can affect leptin (show LEP ELISA Kits) levels and food intake during obesity.
MYSM1 (show MYSM1 ELISA Kits) is a critical negative regulator of p53 (show TP53 ELISA Kits) transcriptional programs in hematopoiesis, and its repression of Bbc3/PUMA expression is essential for multipotent progenitor survival, and partly contributes to maintaining hematopoietic stem cel function.
Bim (show BCL2L11 ELISA Kits) and Puma overlapped apoptosis only partially during physiological apoptotic stage and they were present in non-apoptotic parts of the follicles.
Beta-arrestin 2 (show ARRB2 ELISA Kits) promotes inflammation-induced intestinal epithelial apoptosis through endoplasmic reticulum stress/PUMA in colitis.
Puma is the major mediator of virus-induced Bax (show BAX ELISA Kits)/Bak (show BAK1 ELISA Kits) activation and mitochondrial membrane permeabilization induction.
Oxidative stress increases PUMA expression regulated by FoxO1 (show FOXO1 ELISA Kits) in follicular granulosa cells.
Results indicate that PUMA is involved in the apoptosis of cerebral astrocytes upon ischemia/reperfusion injury
by preventing the consumption of IL-15 (show IL15 ELISA Kits), Bim (show BCL2L11 ELISA Kits) limits the role of Noxa (show PMAIP1 ELISA Kits) and Puma in causing the death of effector cells with less memory potential.
These results demonstrate that antagonism between PUMA and MCL-1 constitutes the major axis of control of hematopoietic stem cell survival.
Bad functions as an essential sensitizer and Puma as an essential activator of IR-induced mitochondrial apoptosis specifically in embryonic neural tissue.
Defective adult oligodendrocyte and Schwann cell development, pigment pattern, and craniofacial morphology in puma mutant zebrafish having an alpha tubulin (show TUBA4A ELISA Kits) mutation
This gene encodes a member of the BCL-2 family of proteins. This family member belongs to the BH3-only pro-apoptotic subclass. The protein cooperates with direct activator proteins to induce mitochondrial outer membrane permeabilization and apoptosis. It can bind to anti-apoptotic Bcl-2 family members to induce mitochondrial dysfunction and caspase activation. Because of its pro-apoptotic role, this gene is a potential drug target for cancer therapy and for tissue injury. Alternative splicing results in multiple transcript variants.
BCL2 binding component 3
, bcl-2-binding component 3
, p53 up-regulated modulator of apoptosis
, Bcl-2 binding component 3