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Therefore, the current findings indicate that Noxa is a novel regulator of early mitosis before 75% epiboly stage when it translates into a key mediator of apoptosis in subsequent embryogenesis.
Noxa demethylation has a role in Bortezomib resistance in mantle cell lymphoma
SATB1 (show SATB1 ELISA Kits) as a Dual Regulator of Anti-Apoptotic BCL2 (show BCL2 ELISA Kits) and Pro-Apoptotic NOXA Genes
ALK-negative anaplastic large cell lymphoma is sensitive to bortezomib through Noxa upregulation and release of Bax (show BAX ELISA Kits) from Bcl-2 (show BCL2 ELISA Kits).
BCL2 (show BCL2 ELISA Kits) and BCLX (show BCL2L1 ELISA Kits) phosphorylation represents a priming event in mitotic cell death that is triggered by NOXA-dependent MCL1 (show MCL1 ELISA Kits) degradation. The MCL1 (show MCL1 ELISA Kits) decay allows in turn BIM (show BCL2L11 ELISA Kits)-dependent cell death.
Overexpression of nonphosphorylatable Noxa resulted in enhanced mitochondria-mediated apoptosis in the infected epithelium.
Results reveal that oncogenic activation of MEK (show MAP2K1 ELISA Kits)/ERK (show EPHB2 ELISA Kits) drives Noxa expression to promote autophagy, and suggest that Noxa has an indirect anti-apoptosis role in melanoma cells under nutrient starvation conditions.
Overall, these data reveal a Noxa-mediated signaling pathway that couples lysosomal membrane permeabilization with mitochondrial outer membrane permeabilization and ultimate apoptosis during oxidative stress.
CDK5 (show CDK5 ELISA Kits) activity provides resistance to heat-induced apoptosis through the expression of miR (show MLXIP ELISA Kits)-23a and subsequent suppression of NOXA synthesis
Mcl-1 (show MCL1 ELISA Kits)/Noxa axis is important to overcome resistance to mitochondrial apoptosis in squamous cell carcinoma.
Cells overexpressing HSP70 (show HSP70 ELISA Kits) had higher levels of miR (show MLXIP ELISA Kits)-23a, maintained these levels after heat shock and accumulated lower levels of NOXA mRNA and protein.
In addition, studies in leukemia Jurkat T cells support the existence of the Sall2 (show SALL2 ELISA Kits)/Noxa axis, and the significance of this axis on the apoptotic response to doxorubicin in cancer cells.
Our data demonstrate that ES cells are uniquely sensitive to CDK1 (show CDK1 ELISA Kits) inhibition via a p53 (show TP53 ELISA Kits)/NOXA/MCL1 (show MCL1 ELISA Kits) pathway.
by preventing the consumption of IL-15 (show IL15 ELISA Kits), Bim (show BCL2L11 ELISA Kits) limits the role of Noxa and Puma (show BBC3 ELISA Kits) in causing the death of effector cells with less memory potential.
Induction of noxa does not influence ischemic neuronal injury.
the current findings indicate that Noxa is a novel regulator of early mitosis before 75% epiboly stage when it translates into a key mediator of apoptosis in subsequent embryogenesis.
Noxa controls expansion of erythroid precursors and RBC (show CACNA1C ELISA Kits) production in vivo under conditions of induced anemia.
Noxa is targeted to the mitochondrial membrane where it neutralises Mcl-1 (show MCL1 ELISA Kits) via its C-terminal BH3-domain.
Induction of senescence was only impaired in cells from the p21-/- puma (show BBC3 ELISA Kits)-/- noxa-/- mice but abrogated in cells from the p53 (show TP53 ELISA Kits)-/- mice.
Oppositional regulation of Noxa by JNK1 (show MAPK8 ELISA Kits) and JNK2 (show MAPK9 ELISA Kits) during apoptosis induced by proteasomal inhibitors.
Promotes activation of caspases and apoptosis. Promotes mitochondrial membrane changes and efflux of apoptogenic proteins from the mitochondria. Contributes to p53/TP53-dependent apoptosis after radiation exposure. Promotes proteasomal degradation of MCL1. Competes with BAK1 for binding to MCL1 and can displace BAK1 from its binding site on MCL1 (By similarity). Competes with BIM/BCL2L11 for binding to MCL1 and can displace BIM/BCL2L11 from its binding site on MCL1.
phorbol-12-myristate-13-acetate-induced protein 1
, PMA-induced protein 1
, adult T cell leukemia-derived PMA-responsive
, immediate-early-response protein APR
, protein Noxa