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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 (show BAK1 Proteins) enrichment at the ER to tether mitochondria for efficient calcium transfer.
These studies suggest a link between Bik-mediated caspase (show CASP3 Proteins) activation and cleavage of viral proteins.
OPN (show SPP1 Proteins) induces oxidative stress via the involvement of mitochondria and NOX-4 (show NOX4 Proteins). 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 (show SQSTM1 Proteins) converts cytoprotective autophagy to an inefficient form due to cargo loading failure, leading to NBK/Bik accumulation, which triggers apoptosis.
Src (show SRC Proteins) tyrosine kinase (show TYRO3 Proteins) inhibits apoptosis through the Erk1/2- dependent degradation of the death accelerator Bik.
The Bik protein, even in combination with Noxa (show PMAIP1 Proteins), is not a potent suppressor of c-Myc (show MYC Proteins)-driven tumourigenesis or critical for chemotherapeutic drug-induced killing of Myc (show MYC Proteins)-driven tumours.
BIKDD, a constitutively active mutant form of proapoptotic gene, BIK, effectively induces apoptosis of breast cancer cells and synergizes with lapatinib.
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 (show BBC3 Proteins) proteins
Data show that Bik and Bim (show BCL2L11 Proteins) share the role of eliminating supernumerary germ cells during the first wave of spermatogenesis, a process vital for normal testicular development.
the results revealed the autophagy modulator TMEM74 interrelates with apoptosis inducer BIK and inhibits its function.
Data suggest that the ERalpha (show ESR1 Proteins)-H19 (show NCKAP1 Proteins)-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 (show ROS1 Proteins) production, BAX (show BAX Proteins) and BAK (show BAK1 Proteins) activation, cytochrome c (show CYCS Proteins) release and caspase (show CASP3 Proteins) activation.
our data demonstrated that suppression of BIK in ER-positive MCF-7 cells prevents the cytotoxic effect of TAM (show CCNA1 Proteins) 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.
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