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anti-Rat (Rattus) BBC3 Antikörper:
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Human Polyclonal BBC3 Primary Antibody für IHC (p), IHC - ABIN252347
Hershko, Ginsberg: Up-regulation of Bcl-2 homology 3 (BH3)-only proteins by E2F1 mediates apoptosis. in The Journal of biological chemistry 2004
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Human Polyclonal BBC3 Primary Antibody für ELISA, ICC - ABIN4348684
Toth, Jeffers, Nickson, Min, Morgan, Zambetti, Erhardt: Targeted deletion of Puma attenuates cardiomyocyte death and improves cardiac function during ischemia-reperfusion. in American journal of physiology. Heart and circulatory physiology 2006
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Polyclonal BBC3 Primary Antibody für WB - ABIN540845
Nakano, Vousden: PUMA, a novel proapoptotic gene, is induced by p53. in Molecular cell 2001
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Human Polyclonal BBC3 Primary Antibody für IHC (p), WB - ABIN541428
Yu, Zhang, Hwang, Kinzler, Vogelstein: PUMA induces the rapid apoptosis of colorectal cancer cells. in Molecular cell 2001
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Human Monoclonal BBC3 Primary Antibody für WB - ABIN534456
Han, Flemington, Houghton, Gu, Zambetti, Lutz, Zhu, Chittenden: Expression of bbc3, a pro-apoptotic BH3-only gene, is regulated by diverse cell death and survival signals. in Proceedings of the National Academy of Sciences of the United States of America 2001
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Polyclonal BBC3 Primary Antibody für WB - ABIN540857
Stylianou, Clarke, Brennan: Aberrant activation of notch signaling in human breast cancer. in Cancer research 2006
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Human Polyclonal BBC3 Primary Antibody für ICC, IF - ABIN153058
Yu, Wang, Kinzler, Vogelstein, Zhang: PUMA mediates the apoptotic response to p53 in colorectal cancer cells. in Proceedings of the National Academy of Sciences of the United States of America 2003
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Authors found that miR-663 regulates apoptosis by controlling mitochondrial outer membrane permeabilization (MOMP) through the expression of two novel direct targets PUMA/BBC3 and BTG2.
LincRNA-p21 is aberrantly upregulated in non-small cell lung cancer and inhibits cell apoptosis by decreasing PUMA expression.
genetic or pharmacological disruption of alphavbeta3/Src signaling drives PUMA expression, specifically depleting these stem-like tumor cells; increases their sensitivity to apoptosis; and reduces pulmonary metastasis, with no effect on primary tumor growth.
TAM improves susceptibility of Beclin-1-deficient glioma cells to CRAd-S-5/3 oncolysis.
Inhibition of aurora kinases preferentially kills mutant KRAS CRC cells and overcomes KRAS-mediated resistance to anti-EGFR antibodies in vitro and in vivo by restoring PUMA induction.
Apoptosis pathways are impaired in fibroblasts from patients with SSc, leading to chronic fibrosis. Nonetheless, PUMA/p53 pathway may not be involved in dysfunction of apoptosis mechanisms in fibroblasts of patients with SSc.
PUMA promotes the cytosolic release of mitochondrial DNA and activation of the DNA sensors DAI/Zbp1 and STING, leading to enhanced RIP3 and MLKL phosphorylation in a positive feedback loop.
miR222 inhibitor exerted anticancer effects against liver cancer cells, probably by targeting the 3' untranslated region (UTR) of BBC3.
PAK1 is upregulated in cutaneous T cell lymphoma. PAK1 silencing induced apoptosis and inhibited cell growth by stimulating the expression of PUMA and p21.
ERK1/2/p53/PUMA signaling axis is related to cisplatin-induced cell death in ovarian cancer cells.
these results establish a critical role of PUMA in mediating the anticancer effects of deguelin in lung cancer cells and provide the rationale for clinical evaluation.
AGG is also found to trigger ubiquitination of PUMA which in turn interacted with p62 for prompting mitophagy suggesting that AGG turns on PUMA-mediated mitophagy in U87MG cells in both p62-dependent as well as in p62-independent manner
Low PUMA expression is associated with cancer.
Authors show that blockade of cAMP signaling using MDL12330A led to an increase in PUMA transcript levels, but not p21 in melanoma cells. Results suggest that transcriptional repression is one of the functions of the cAMP-Epac signaling pathway.
Altogether, these findings suggest that in normal/high glucose condition a mutual unbalance between p53-dependent apoptosis (PUMA) and autophagy (DRAM) gene occurred, modifying the ADR-induced cancer cell death in HG both in vitro and in vivo.
Data suggest that H2O2 regulates cell death in granulosa cells via the ROS-JNK-p53 pathway.
Collectively, our findings strongly suggest targeting miR-155 exhibited in vivo and in vitro antileukemic activities in acute myelogeneous leukemia through a novel mechanism resulting in inhibition of Slug expression and increase of PUMA expression.
these results establish a critical role of PUMA in mediating the anticancer effects of pazopanib in colon cancer cells and provide the rationale for clinical evaluation.
Concurrent knock-down of Puma reverses Bcl-xl-induced caspase activation. Puma is required for Bclxl-induced cell death.
Knockdown of Slug enhanced the antitumor activity of DOX in SW1736 cells via induction of PUMA upregulation. Our results suggest that targeting of Slug has good potential for the development of new therapeutic strategies for Anaplastic thyroid carcinoma.
Using gain- and loss-of-function approaches, we identified a unique role of miR-143/PUMA in mediating microglial activation via regulation of NLRP3 inflammasome activation.
Expression from a luciferase reporter construct containing the 2 kb fragment of the promoter region of bcl-2-binding component 3 (PUMA) is enhanced by activation of the muscle regulatory transcription factor MyoD in both myoblasts and fibroblasts and diminishes by silencing of MyoD in myoblasts. E-Box Sequences at position - 857 of PUMA is the binding site for MyoD.
Proapoptotic proteins BIM and PUMA are not critical for the reticulocyte apoptosis caused by loss of the pro-survival protein BCL-XL.
The mitochondrial apoptotic pathway, activated by BH3-only proteins, BIM and PUMA, is essential for endoplasmic reticulum stress-induced cell death; DR5 as well as caspase-8 are not required for this process.
Mir143-BBC3 has roles in microglial survival in the context of drug abuse
In the mouse model of silicosis, Bbc3 knockout mice clearly exhibited decreased levels of autophagy and fibrosis progression. These results suggest that downregulation of BBC3 expression may become a novel therapeutic strategy for the treatment of silicosis.
This study has demonstrated that methamphetamine-mediated pericytes migration involves PUMA up-regulation.
Data show that Emu-Myc mice lacking both p21 and PUMA developed lymphoma at a rate considerably longer latency than Emu-Myc;p53(+/-)mice.
Our data show a novel pathway of infection-induced apoptosis that enhances our understanding of the mechanism by which BH3-only proteins control apoptotic host cell death during Listeria infection.
Overexpression of miR-29 or miR-24 is sufficient to inhibit the induction of Bim and Puma in young sympathetic neurons.
loss of PUMA had no impact on the loss of platelets caused by loss of BCL-XL. It therefore remains to be established whether other BH3-only proteins play a critical role in induction of apoptosis in platelets or whether their death is controlled solely by the interactions between BCL-XL with BAK and BAX.
PUMA is dispensable for glucose homeostasis in lean and obese mice, but it can affect leptin levels and food intake during obesity.
MYSM1 is a critical negative regulator of p53 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.
Therapeutic response to non-genotoxic activation of p53 by Nutlin3a is driven by PUMA-mediated apoptosis in lymphoma cells.
Bim and Puma overlapped apoptosis only partially during physiological apoptotic stage and they were present in non-apoptotic parts of the follicles.
Beta-arrestin 2 promotes inflammation-induced intestinal epithelial apoptosis through endoplasmic reticulum stress/PUMA in colitis.
Puma is the major mediator of virus-induced Bax/Bak activation and mitochondrial membrane permeabilization induction.
Oxidative stress increases PUMA expression regulated by FoxO1 in follicular granulosa cells.
Results indicate that PUMA is involved in the apoptosis of cerebral astrocytes upon ischemia/reperfusion injury
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 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