The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Use a concentration of 0.5 - 1 µg/ml. Detects a band of approximately 177 kDa (predicted molecular weight: 171 kDa).
Staining of the WSTF band in immunoblotting is specifically inhibited by the immunizing peptide.
Use at an assay dependent concentration.
5-10 µg immunoprecipitates WSTF from lysates of HEK293-T cells.
Atypical tyrosine-protein kinase that plays a central role in chromatin remodeling and acts as a transcription regulator. Involved in DNA damage response by phosphorylating 'Tyr-142' of histone H2AX (H2AXY142ph). H2AXY142ph plays a central role in DNA repair and acts as a mark that distinguishes between apoptotic and repair responses to genotoxic stress. Essential component of the WICH complex, a chromatin remodeling complex that mobilizes nucleosomes and reconfigures irregular chromatin to a regular nucleosomal array structure. The WICH complex regulates the transcription of various genes, has a role in RNA polymerase I and RNA polymerase III transcription, mediates the histone H2AX phosphorylation at 'Tyr-142', and is involved in the maintenance of chromatin structures during DNA replication processes. In the complex, it mediates the recruitment of the WICH complex to replication foci during DNA replication. Also involved in vitamin D-coupled transcription regulation via its association with the WINAC complex, a chromatin-remodeling complex recruited by vitamin D receptor (VDR), which is required for the ligand-bound VDR-mediated transrepression of the CYP27B1 gene. In the WINAC complex, plays an essential role by targeting the complex to acetylated histones, an essential step for VDR-promoter association.
Ubiquitously expressed with high levels of expression in heart, brain, placenta, skeletal muscle and ovary.
Involvement in disease
Note=BAZ1B is located in the Williams-Beuren syndrome (WBS) critical region. WBS results from a hemizygous deletion of several genes on chromosome 7q11.23, thought to arise as a consequence of unequal crossing over between highly homologous low-copy repeat sequences flanking the deleted region. Haploinsufficiency of BAZ1B may be the cause of certain cardiovascular and musculo-skeletal abnormalities observed in the disease.
Lalli MA et al. Haploinsufficiency of BAZ1B contributes to Williams syndrome through transcriptional dysregulation of neurodevelopmental pathways. Hum Mol Genet25:1294-306 (2016).
Read more (PubMed: 26755828) »
Geiger R et al. L-Arginine Modulates T Cell Metabolism and Enhances Survival and Anti-tumor Activity. Cell167:829-842.e13 (2016).
Read more (PubMed: 27745970) »