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PTEN and PMAIP1 are targets of miR-26a-5p and let-7g-5p, respectively.
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.
Our data showed that Bmi1 is highly expressed in human non-small cell lung cancer (NSCLC) tissues and cell lines. Knockdown of Bmi1 significantly suppressed NSCLC cell proliferation and colony formation. Deguelin treatment attenuated the binding activity of Bmi1 to the Noxa promoter, thus resulting in Noxa transcription and apoptosis activation
BIM and NOXA contribute to TAF6delta-dependent cell death.
HHT and bortezomib cooperate to kill DLBCL and MCL cells through a process involving MCL-1 down-regulation, NOXA up-regulation.
Pharmacologic induction of NOXA, using the histone deacetylase inhibitor panobinostat, decreased MCL1 protein abundance and increased lymphoma cell vulnerability to BCL2 inhibitors in vitro and in vivo.
Data report that NOXA is a physiological substrate of autophagy. Mechanistic studies revealed that NOXA is hijacked by p62 for degradation during the autophagic process, and the three lysine residues at the C-terminus of NOXA are required for its autophagic degradation. Furthermore, autophagy can block apoptosis by eliminating NOXA in both p53-dependent and p53-independent manners.
Fluorizoline increased the protein levels of the pro-apoptotic B-cell lymphoma 2 family member NOXA in chronic lymphocytic leukemia cells. Furthermore, fluorizoline synergized with ibrutinib, 5-aminoimidazole-4-carboxamide riboside or venetoclax to induce apoptosis.
By ubiquitylating and degrading NOXA through activating CRL5, UBE2F selectively promotes lung cancer cell survival and could, therefore, serve as a novel cancer target
Data show that Noxa-mediated MCL-1 phosphorylation and degradation is regulated by CDK2.
the c-FLIP and NOXA/Mcl-1 axis participated in the synergistic effect of pemetrexed plus cisplatin in human choroidal melanoma cells
Noxa is involved in X-ray-induced lung injury.
Arsenic trioxide induces Noxa-dependent apoptosis in rhabdomyosarcoma cells and acts synergistically with antimicrotubule drugs.
knockdown of MCL-1 in MRT cell lines induced apoptosis and increased DOX sensitivity in malignant rhabdoid tumor cells
high levels of miR21 expression may induce gastric cancer migration and invasion via the downregulation of Noxa expression
Inhibition of SIRT1 could induce the Noxa expression in A549/DDP cells.
Fluorizoline bind to prohibitin, inducing mitochondrial apoptotic pathway through NOXA and BIM upregulation.
Noxa demethylation has a role in Bortezomib resistance in mantle cell lymphoma
SATB1 as a Dual Regulator of Anti-Apoptotic BCL2 and Pro-Apoptotic NOXA Genes
ALK-negative anaplastic large cell lymphoma is sensitive to bortezomib through Noxa upregulation and release of Bax from Bcl-2.
BCL2 and BCLX phosphorylation represents a priming event in mitotic cell death that is triggered by NOXA-dependent MCL1 degradation. The MCL1 decay allows in turn BIM-dependent cell death.
Overexpression of nonphosphorylatable Noxa resulted in enhanced mitochondria-mediated apoptosis in the infected epithelium.
Findings indicate that prospero homeobox 1 (Prox1) regulated the differentiation of oligodendrocyte precursor cells via the regulation of phorbol-12-myristate-13-acetate-induced protein 1 (NOXA).
data suggest that in the context of CLL NOXA may function as an oncomodulator
knockdown of pmaip1 mimicked the phenotype of ph8(-/Y) by showing the decreased apoptosis during early differentiation of embryonic stem cells and promoted mesodermal and cardiac commitment.
In vivo upregulation of noxa was reduced by pifithrin-alpha, suggesting transcription may be partly p53-dependent.The present findings indicate Noxa does not serve as a proapoptotic BH3-only protein during seizure-induced neuronal death in vivo
In addition, studies in leukemia Jurkat T cells support the existence of the Sall2/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 inhibition via a p53/NOXA/MCL1 pathway.
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.
by preventing the consumption of IL-15, Bim limits the role of Noxa and Puma 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 production in vivo under conditions of induced anemia.
Noxa is targeted to the mitochondrial membrane where it neutralises Mcl-1 via its C-terminal BH3-domain.
Induction of senescence was only impaired in cells from the p21-/- puma-/- noxa-/- mice but abrogated in cells from the p53-/- mice.
Oppositional regulation of Noxa by JNK1 and JNK2 during apoptosis induced by proteasomal inhibitors.
In acute viral infection, Noxa(-/-) mice had increased memory pool size & diversity but less cross-reactivity. Reduced T-cell apoptosis during chronic activation led to severe organ pathology & early death.
Data show that PUMA and NOXA are critical for DNA damage-induced, TAp63-mediated primordial follicle oocyte apoptosis.
Results suggest that compromised induction of Unfolded Protein Response (UPR) and increased NOXA expression contributes to hypersensitivity of PERK(-/-) MEFs to ER stress-induced apoptosis.
two proapoptotic Bcl-2 family members Bok and Noxa/Pmaip are directly transcriptionally induced by activated MAL and upon activation of the actin-MAL-SRF pathway
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