Anti-INI-1/SNF5

SNF5/INI1 is the core subunit of the SWI/SNF chromatin remodeling complex that contributes to the regulation of chromatin structure. It is a tumor suppressor in humans and mice, with an essential role in early embryonic development. SNF5 interacts with UV damage recognition factor XPC and colocalizes at the damage site upon UV irradiation. Inactivation of SNF5 affects the recruitment of ATM checkpoint kinase to the damage site and ATM activation by phosphorylation. SNF5 deficiency results in a defect in H2AX and BRCA1 phosphorylation at the damage site. SNF5/INI1 forms a functional complex with p300/GATA4 on hypertrophic response gene promoters in cardiomyocytes. It plays an inhibitory role in cardiomyocyte hypertrophy by suppressing p300/GATA4-dependent transcription. SNF5 genetic mutations were first reported in malignant rhabdoid tumors. Protein function: Core component of the BAF (hSWI/SNF) complex. This ATP- dependent chromatin-remodeling complex plays important roles in cell proliferation and differentiation, in cellular antiviral activities and inhibition of tumor formation. The BAF complex is able to create a stable, altered form of chromatin that constrains fewer negative supercoils than normal. This change in supercoiling would be due to the conversion of up to one-half of the nucleosomes on polynucleosomal arrays into asymmetric structures, termed altosomes, each composed of 2 histones octamers. Stimulates in vitro the remodeling activity of SMARCA4/BRG1/BAF190A. Involved in activation of CSF1 promoter. Belongs to the neural progenitors- specific chromatin remodeling complex (npBAF complex) and the neuron-specific chromatin remodeling complex (nBAF complex). During neural development a switch from a stem/progenitor to a postmitotic chromatin remodeling mechanism occurs as neurons exit the cell cycle and become committed to their adult state. The transition from proliferating neural stem/progenitor cells to postmitotic neurons requires a switch in subunit composition of the npBAF and nBAF complexes. As neural progenitors exit mitosis and differentiate into neurons, npBAF complexes which contain ACTL6A/BAF53A and PHF10/BAF45A, are exchanged for homologous alternative ACTL6B/BAF53B and DPF1/BAF45B or DPF3/BAF45C subunits in neuron-specific complexes (nBAF). The npBAF complex is essential for the self-renewal/proliferative capacity of the multipotent neural stem cells. The nBAF complex along with CREST plays a role regulating the activity of genes essential for dendrite growth. Plays a key role in cell-cycle control and causes cell cycle arrest in G0/G1. [The UniProt Consortium]