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Human Polyclonal BAK1 Primary Antibody für IHC, ELISA - ABIN1533215
Plötz, Gillissen, Hossini, Daniel, Eberle: Disruption of the VDAC2-Bak interaction by Bcl-x(S) mediates efficient induction of apoptosis in melanoma cells. in Cell death and differentiation 2012
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Human Polyclonal BAK1 Primary Antibody für IF (p), IHC (p) - ABIN674409
Zhu, Wang, Liang, Wang, Zhang, Li, Ying: Regulation of cell transformation by Rb-controlled redox homeostasis. in PLoS ONE 2014
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Human Polyclonal BAK1 Primary Antibody für ELISA, WB - ABIN257856
Derry, Ochs, Francke: Isolation of a novel gene mutated in Wiskott-Aldrich syndrome. in Cell 1994
Human Polyclonal BAK1 Primary Antibody für IHC, IHC (p) - ABIN4282996
Krajewska, Rosenthal, Mikolajczyk, Stennicke, Wiesenthal, Mai, Naito, Salvesen, Reed, Fiskum, Krajewski: Early processing of Bid and caspase-6, -8, -10, -14 in the canine brain during cardiac arrest and resuscitation. in Experimental neurology 2004
Human Polyclonal BAK1 Primary Antibody für WB - ABIN2801911
Farrow, White, Martinou, Raven, Pun, Grinham, Martinou, Brown: Cloning of a bcl-2 homologue by interaction with adenovirus E1B 19K. in Nature 1995
BIR3 interacts with BAK1 and inhibits ligand binding receptors to prevent BAK1 receptor complex formation.
The role of BAK1 in defense against root-knot (zeige KCNK7 Antikörper) nematode and pattern-triggered immunity
N-glycosylation and specific ERQC components are essential to activate bak1/serk4 cell death, and CRK4 is likely to be among client proteins of protein glycosylation involved in BAK1/SERK4-regulated cell death.
BAK1 and SOBIR1 associate with each other in planta when the function of BIR1 (zeige KCNJ6 Antikörper) is compromised.
an allosteric mechanism for inhibition of BAK1 by C408 S-glutathionylation
Study identifies a link between plant perception of biotic threats by BAK1, cellular calcium entry mediated by GLRs, and intracellular calcium release by TPC1 (zeige TPCN1 Antikörper) during a biologically relevant interaction.
The Arabidopsis Malectin (zeige MLEC Antikörper)-Like/LRR-RLK (zeige TXK Antikörper) IOS1 Is Critical for BAK1-Dependent and BAK1-Independent Pattern-Triggered Immunity
These findings show that BAK1 contains an additional AtRALF1 binding site, indicating that this protein may be part of a AtRALF1-containing complex as a co-receptor, and it is required for the negative regulation of cell expansion
the existence of partial redundancy between SERK3 and SERK1 as well as the promoting or repressive activity of a single coreceptor in multiple simultaneously active pathways, is reported.
The found that in an otherwise "active" BAK1 the alphaC helix is highly disordered, a hallmark of deactivation, whereas the BRI1 alphaC helix is moderately disordered and displays swinging behavior similar to numerous animal kinases.
interleukin-6 (zeige IL6 Antikörper), endothelin ET-1 (zeige EDN1 Antikörper), and apoptotic Bak and Bcl-XL (zeige BCL2L1 Antikörper) genes have roles in small bowel transplantation, in a swine model of ischemia and reperfusion injury
Bak mRNA was significantly increased in haploid parthenotes compared with the diploid parthenotes. These results suggest that the haploid state affects apoptosis-related gene expression which results in increased apoptosis
This comprehensive survey showed that in each Bak dimer the N-termini are fully solvent-exposed and mobile, the core is highly structured, and the C-termini are flexible but restrained by their contact with the membrane.
The BAK1/BCL2 (zeige BCL2 Antikörper) ratio was positively correlated with the results of audiometric tests. Our results indicate that BAK-mediated apoptosis may be a core mechanism in the progression of age-related hearing impairment in humans
UMI-77 enhances TRAIL-induced apoptosis by unsequestering Bim (zeige BCL2L11 Antikörper) and Bak, which provides a novel therapeutic strategy for the treatment of gliomas.
after the induction of apoptosis, Bak switches from its association with Mtx2 (zeige MTX2 Antikörper) and VDAC2 (zeige VDAC2 Antikörper) to a closer association with Mtx1 (zeige MTX1 Antikörper).
Conversion of Bim (zeige BCL2L11 Antikörper)-BH3 from Activator to Inhibitor of Bak through Structure-Based Design.
The results strongly suggest that the direct apoptosis-activation activities of Bid (zeige BID Antikörper), Bim (zeige BCL2L11 Antikörper), Puma (zeige BBC3 Antikörper), and p53 (zeige TP53 Antikörper) are not essential for activating Bax (zeige BAX Antikörper)/Bak once the anti-apoptotic Bcl-2 (zeige BCL2 Antikörper) proteins are neutralized.
Studied BAK1, SPRY4 (zeige SPRY4 Antikörper) and GAB2 (zeige GAB2 Antikörper) SNPs in pediatric germ cell tumors(GCT (zeige QPCT Antikörper)); found a variant in SPRY4 (zeige SPRY4 Antikörper) was associated with reduced risk of GCT (zeige QPCT Antikörper); a variant in BAK1 was positively associated with GCT (zeige QPCT Antikörper) with a strong estimated effect for testis tumors; and a SNP in GAB2 (zeige GAB2 Antikörper) was associated with increased risk for GCT (zeige QPCT Antikörper).
These results not only establish Bok (zeige BOK Antikörper) as a Bak- and Bax (zeige BAX Antikörper)-independent apoptosis inducer, but also suggest a potential impact of Bok (zeige BOK Antikörper) expression in ovarian cancer therapy.
The low-level constitutive production of platelets caused by the G allele of rs5745568 in BAK1 protein seems to increase the risk of bleeding in dengue infection
the expression of Bak1 was downregulated in CRC (zeige CALR Antikörper) tumor tissues and was reversely correlated with the expression of miR410, which provided further support that Bak1 was regulated by miR410.
Here the authors show that mouse embryonic fibroblasts deficient in Bax (zeige BAX Antikörper)/Bak1 are resistant to the third major form of cell death associated with autophagy through a mechanism involving lysosome permeability.
BH3-only (zeige BBC3 Antikörper) proteins bind inactive full-length BAK at mitochondria and then dissociate following exposure of the BAK BH3 and BH4 domains before BAK homodimerization
Resultdetermined the mouse Bak BH3-in-groove homodimers (BGH) structure, which allowed more accurate modeling within and between the BGHs. The BGHs were shown to oligomerize via the 'alpha 3/alpha 5 interface' in mitochondria. These findings suggest for a probable assembly of the Bak homodimers in the mitochondrial apoptotic pore.
We propose that the GC-induced mitochondrial accumulation of Bax (zeige BAX Antikörper) and the interaction between the GR and Bim (zeige BCL2L11 Antikörper), Bcl-xL (zeige BCL2L1 Antikörper) and Bak could play a role in the regulation of thymocyte apoptosis.
Postnatal synaptic rearrangement needed for acquisition of skilled behaviors requires the activity-dependent, non-apoptotic Bax (zeige BAX Antikörper)/Bak-caspase (zeige CASP3 Antikörper) signaling cascade. Adult Bax (zeige BAX Antikörper)/Bak mutant mice exhibit aberrant co-activation of antagonistic muscle pairs and skilled grasping deficits but normal reaching and retrieval behaviors.
The authors show that Bak is activated and that activated Bak is bound to p53 (zeige TP53 Antikörper) during reovirus encephalitis.
Pancreatic beta-Cell Death due to Pdx-1 (zeige PDX1 Antikörper) Deficiency Requires Multi-BH Domain Protein Bax (zeige BAX Antikörper) but Not Bak.
lipid profile in the absence of the proapoptotic proteins BAX (zeige BAX Antikörper) and BAK in mouse embryonic fibroblasts
alpha1 dissociation is a key step in unfolding Bak into three major components, the N terminus, the core (alpha2-alpha5) and the latch (alpha6-alpha8) that is required for apoptosis.
regulation of A1 and Bak contribute to mitochondrial membrane stability, reduced caspase-9 (zeige CASP9 Antikörper) activity, and delayed apoptosis in bovine neutrophils exposed to glucocorticoids
The protein encoded by this gene belongs to the BCL2 protein family. BCL2 family members form oligomers or heterodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. This protein localizes to mitochondria, and functions to induce apoptosis. It interacts with and accelerates the opening of the mitochondrial voltage-dependent anion channel, which leads to a loss in membrane potential and the release of cytochrome c. This protein also interacts with the tumor suppressor P53 after exposure to cell stress.
BCL2-like 7 protein
, apoptosis regulator BAK
, bcl-2 homologous antagonist/killer
, bcl-2-like protein 7
, pro-apoptotic protein BAK
, Bcl2 homologous antagonist/killer
, Bcl-2-like 7