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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.
Fluorizoline bind to prohibitin (show PHB Proteins), inducing mitochondrial apoptotic pathway through NOXA and BIM (show BCL2L11 Proteins) upregulation.
Noxa demethylation has a role in Bortezomib resistance in mantle cell lymphoma
SATB1 (show SATB1 Proteins) as a Dual Regulator of Anti-Apoptotic BCL2 (show BCL2 Proteins) and Pro-Apoptotic NOXA Genes
ALK-negative anaplastic large cell lymphoma is sensitive to bortezomib through Noxa upregulation and release of Bax (show BAX Proteins) from Bcl-2 (show BCL2 Proteins).
BCL2 (show BCL2 Proteins) and BCLX (show BCL2L1 Proteins) phosphorylation represents a priming event in mitotic cell death that is triggered by NOXA-dependent MCL1 (show MCL1 Proteins) degradation. The MCL1 (show MCL1 Proteins) decay allows in turn BIM (show BCL2L11 Proteins)-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 Proteins)/ERK (show EPHB2 Proteins) 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 Proteins) activity provides resistance to heat-induced apoptosis through the expression of miR (show MLXIP Proteins)-23a and subsequent suppression of NOXA synthesis
Mcl-1 (show MCL1 Proteins)/Noxa axis is important to overcome resistance to mitochondrial apoptosis in squamous cell carcinoma.
In addition, studies in leukemia Jurkat T cells support the existence of the Sall2 (show SALL2 Proteins)/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 Proteins) inhibition via a p53 (show TP53 Proteins)/NOXA/MCL1 (show MCL1 Proteins) pathway.
by preventing the consumption of IL-15 (show IL15 Proteins), Bim (show BCL2L11 Proteins) limits the role of Noxa and Puma (show BBC3 Proteins) 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 Proteins) production in vivo under conditions of induced anemia.
Noxa is targeted to the mitochondrial membrane where it neutralises Mcl-1 (show MCL1 Proteins) via its C-terminal BH3-domain.
Induction of senescence was only impaired in cells from the p21-/- puma (show BBC3 Proteins)-/- noxa-/- mice but abrogated in cells from the p53 (show TP53 Proteins)-/- mice.
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