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Bcl-2 interacting killer (Bik) decreases airway epithelial hyperplasia via apoptosis mediated by calcium release from the endoplasmic reticulum (ER), but the mechanism is unclear. Here the authors show that Bik promotes Bak enrichment at the ER to tether mitochondria for efficient calcium transfer.
These studies suggest a link between Bik-mediated caspase activation and cleavage of viral proteins.
OPN induces oxidative stress via the involvement of mitochondria and NOX-4. It may affect mitochondrial morphology and integrity, at least in part, via the involvement of BIK.
Findings identify novel cross talk between autophagy and apoptosis, wherein targeting SQSTM1/p62 converts cytoprotective autophagy to an inefficient form due to cargo loading failure, leading to NBK/Bik accumulation, which triggers apoptosis.
Src tyrosine kinase inhibits apoptosis through the Erk1/2- dependent degradation of the death accelerator Bik.
The Bik protein, even in combination with Noxa, is not a potent suppressor of c-Myc-driven tumourigenesis or critical for chemotherapeutic drug-induced killing of Myc-driven tumours.
BIKDD, a constitutively active mutant form of proapoptotic gene, BIK, effectively induces apoptosis of breast cancer cells and synergizes with lapatinib.
Data show that the apoptotic gene BikDD, not only caused cytotoxic effects in cancer cells but also elicited a cancer-specific cytotoxic T lymphocyte response.
Blk has been mapped to chromosome 15 and overexpressed in transitional B cells of A/WySnJ mice, which demonstrate a cell-autonomous defect leading to excessive apoptosis.
any function of Bik in programmed cell death and stress-induced apoptosis must overlap that of other BH3-only proteins
Data show that Bik and Bim share the role of eliminating supernumerary germ cells during the first wave of spermatogenesis, a process vital for normal testicular development.
Targeted expression of BikDD, a potent proapoptotic gene driven by CCKAR-VISA, exhibited antitumor effects on pancreatic cancer and prolonged survival in multiple xenograft and syngeneic mouse models of pancreatic tumors with virtually no toxicity
evaluated the inhibitory effect of BikDD on the growth kinetics of intraperitoneally inoculated CT-26-Luc
Enhanced expression in Bcl-2 deficient cells leads to cell death with autophagic features.
the results revealed the autophagy modulator TMEM74 interrelates with apoptosis inducer BIK and inhibits its function.
Data suggest that the ERalpha-H19-BIK signaling axis plays an important role in promoting breast cancer cell chemoresistance.
Suggest complex mechanism of tumor promotion in Bik high breast tumors.
BIK significantly contributes to DNA damage-induced mitochondrial apoptosis in HCT-116 wt cells upstream of the second peak of ROS production, BAX and BAK activation, cytochrome c release and caspase activation.
our data demonstrated that suppression of BIK in ER-positive MCF-7 cells prevents the cytotoxic effect of TAM and favors a more aggressive phenotype, due to the molecular change of different pathways
HCV RNA replication and release were significantly suppressed in BIK-depleted cells and over-expression of the RNA-dependent RNA polymerase, NS5B, was able to induce BIK expression
BikDDA, a novel mutant of Bik, showed a prolonged half-life and enhanced pro-apoptotic ability in triple-negative breast cancer cells compared with BikDD.
Authors show that human herpesvirus 4 EBNA2 represses BIK in B-cell lymphoma-derived cell lines and that this host-virus interaction can inhibit the proapoptotic effect of transforming growth factor beta1.
Data suggest BIK expression in tumor cells is not subject to direct regulation by MAP kinase signaling; BIK expression appears to be cell-cycle-dependent and increases in G1 cell-cycle arrest which results from inhibition of MAP kinase signaling.
BIK/NBK gene expression may have important clinical implications and provide predictive, prognostic or therapeutic marker in breast cancer patients
A previously undescribed indirect epigenetic regulation of BIK in FA-C lymphoblasts is mediated by DeltaNp73, an isoform of p73 lacking its transactivation domain that activates BIK through a proximal element in its promoter.
Data indicate that methylation-induced transcriptional silencing of the BIK (bcl2-interacting killer) pro-apoptotic gene may occur in multiple myeloma (MM), which might serve as a predictor of the development of relapsed/refractory MM.
Data show that association of study-wide significance (P < 8.2 x 10(-5)) was identified for single-nucleotide polymorphisms (SNP) in TP53, LIG1, and BIK.
GRP78 can decrease BCL-2 sequestration by BIK at the endoplasmic reticulum
Bik has a role in both, apoptosis induction and sensitivity to oxidative stress in myeloma cells.
genetic polymorphism in patients with ataxia telangiectasia is associated with the disease progression
Systemic tumor suppression by the proapoptotic gene bik.
The protein encoded by this gene shares a critical BH3 domain with other death-promoting proteins, such as BID, BAK, BAD and BAX, that is required for its pro-apoptotic activity, and for interaction with anti-apoptotic members of the BCL2 family, and viral survival-promoting proteins. Since the activity of this protein is suppressed in the presence of survival-promoting proteins, it is suggested as a likely target for anti-apoptotic proteins.
BCL2-interacting killer (apoptosis-inducing)
, BCL2-interacting killer
, apoptosis inducer NBK
, bcl-2-interacting killer
, bik-like killer protein
, apoptosis-inducing NBK