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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.
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.
Activation of p38 (show CRK ELISA Kits) and Jun kinase (show MAPK9 ELISA Kits) results in increased expression of the pro-apoptotic Bcl-2 (show BCL2 ELISA Kits) homologs Bim (show BCL2L11 ELISA Kits) and Puma, which inducibly bind and sequester Mcl-1 (show MCL1 ELISA Kits) and Bcl-xL (show BCL2L1 ELISA Kits) leading to the induction of the mitochondrial apoptosis pathway.
Decrease of survivin (show BIRC5 ELISA Kits) expression and induction of PUMA expression.
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.
caspase-9 (show CASP9 ELISA Kits) mediates Puma activation to determine the threshold for overcoming chemoresistance in cancer cells.
Stable knockdown of Bim (show BCL2L11 ELISA Kits) or PUMA expression prevented cell toxicity induced by loss of Keap1 (show KEAP1 ELISA Kits).
Loss of Bbc3 results in prolonged fertility.
c-Jun (show JUN ELISA Kits) transactivates Puma gene expression to promote osteoarthritis.
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