anti-BIK (BIK) Antikörper

Mouse (Murine) BCL2-Interacting Killer (Apoptosis-Inducing) (BIK) Interaktionspartner

1. 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 (zeige BAK1 Antikörper) enrichment at the ER to tether mitochondria for efficient calcium transfer.

2. These studies suggest a link between Bik-mediated caspase (zeige CASP3 Antikörper) activation and cleavage of viral proteins.

3. OPN (zeige SPP1 Antikörper) induces oxidative stress via the involvement of mitochondria and NOX-4 (zeige NOX4 Antikörper). It may affect mitochondrial morphology and integrity, at least in part, via the involvement of BIK.

4. Findings identify novel cross talk between autophagy and apoptosis, wherein targeting SQSTM1/p62 (zeige SQSTM1 Antikörper) converts cytoprotective autophagy to an inefficient form due to cargo loading failure, leading to NBK/Bik accumulation, which triggers apoptosis.

5. Src (zeige SRC Antikörper) tyrosine kinase (zeige TYRO3 Antikörper) inhibits apoptosis through the Erk1/2- dependent degradation of the death accelerator Bik.

6. The Bik protein, even in combination with Noxa (zeige PMAIP1 Antikörper), is not a potent suppressor of c-Myc (zeige MYC Antikörper)-driven tumourigenesis or critical for chemotherapeutic drug-induced killing of Myc (zeige MYC Antikörper)-driven tumours.

7. BIKDD, a constitutively active mutant form of proapoptotic gene, BIK, effectively induces apoptosis of breast cancer cells and synergizes with lapatinib.

8. 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.

9. any function of Bik in programmed cell death and stress-induced apoptosis must overlap that of other BH3-only (zeige BBC3 Antikörper) proteins

10. Data show that Bik and Bim (zeige BCL2L11 Antikörper) share the role of eliminating supernumerary germ cells during the first wave of spermatogenesis, a process vital for normal testicular development.

Human BCL2-Interacting Killer (Apoptosis-Inducing) (BIK) Interaktionspartner

1. the results revealed the autophagy modulator TMEM74 (zeige TMEM74 Antikörper) interrelates with apoptosis inducer BIK and inhibits its function.

2. Data suggest that the ERalpha (zeige ESR1 Antikörper)-H19 (zeige NCKAP1 Antikörper)-BIK signaling axis plays an important role in promoting breast cancer cell chemoresistance.

3. Suggest complex mechanism of tumor promotion in Bik high breast tumors.

4. BIK significantly contributes to DNA damage-induced mitochondrial apoptosis in HCT-116 wt cells upstream of the second peak of ROS (zeige ROS1 Antikörper) production, BAX (zeige BAX Antikörper) and BAK (zeige BAK1 Antikörper) activation, cytochrome c (zeige CYCS Antikörper) release and caspase (zeige CASP3 Antikörper) activation.

5. These studies suggest a link between Bik-mediated caspase (zeige CASP3 Antikörper) activation and cleavage of viral proteins.

6. our data demonstrated that suppression of BIK in ER-positive MCF-7 cells prevents the cytotoxic effect of TAM (zeige CCNA1 Antikörper) and favors a more aggressive phenotype, due to the molecular change of different pathways

7. 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

8. 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.

9. Findings identify novel cross talk between autophagy and apoptosis, wherein targeting SQSTM1/p62 (zeige SQSTM1 Antikörper) converts cytoprotective autophagy to an inefficient form due to cargo loading failure, leading to NBK/Bik accumulation, which triggers apoptosis.

10. 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.