Bit1 polyclonal, anti-human, mouse, rat
€396.00
In stock
SKU
253558
Catalog Nr.: 253558
Size: 0.1 mg
Isotype: Rabbit Ig
Applications: E, WB, ICC
Size: 0.1 mg
Isotype: Rabbit Ig
Applications: E, WB, ICC
Protein Family: Enzymes
Pathway and Disease: Signaling Molecules and Interaction
Description:
Adhesion to extracellular matrix regulates cell survival through both integrin engagement and appropriate cell spreading. Anoikis is the molecular mechanism of apoptosis induced by integrin detachment. Bit1 (Bcl-2 inhibitor of transcription 1) was recently identified as being involved in this process. Bit1 is a mitochondrial protein that is released into the cytoplasm upon onset of apoptosis where it forms a complex with AES, a small Groucho/transducin-like enhancer of split (TLE) protein and induces caspase-independent apoptosis. Both AES and TLE proteins are transcriptional co-repressors that play important roles in neurogenesis, segmentation, and sex determination. It has been suggested that Bit1-AES complexes turn off a survival-promoting gene transcription program controlled by TLE. Interestingly, apoptosis of cells transfected with Bit1 and AES could be inhibited if the cells were allowed to attach to fibronectin through the alpha5beta1 integrin suggesting that the Bit1-AES pathway contributing to anoikis is regulated by integrins, and in particular, the alpha5beta1 integrin.
Alternate Names: Bit1 , Bcl-2 inhibitor of transcription 1 / Peptidyl-tRNA hydrolase 2
Application Notes: E: 1:500-1:1,000; WB: 1:100-1:500; ICC: 1:100-1:500
Accession No.: NP_057161
Antigen: KLH-conjugated synthetic peptide encompassing a sequence within human BIT1.
Format: Each vial contains 0.1 ml IgG in PBS pH 7.4 with 0.02% sodium azide. Antibody was purified by immunogen affinity chromatography.
Storage:
Store at -20°C. Minimize freeze-thaw cycles. Product is guaranteed one year from the date of shipment.
Pathway and Disease: Signaling Molecules and Interaction
Description:
Adhesion to extracellular matrix regulates cell survival through both integrin engagement and appropriate cell spreading. Anoikis is the molecular mechanism of apoptosis induced by integrin detachment. Bit1 (Bcl-2 inhibitor of transcription 1) was recently identified as being involved in this process. Bit1 is a mitochondrial protein that is released into the cytoplasm upon onset of apoptosis where it forms a complex with AES, a small Groucho/transducin-like enhancer of split (TLE) protein and induces caspase-independent apoptosis. Both AES and TLE proteins are transcriptional co-repressors that play important roles in neurogenesis, segmentation, and sex determination. It has been suggested that Bit1-AES complexes turn off a survival-promoting gene transcription program controlled by TLE. Interestingly, apoptosis of cells transfected with Bit1 and AES could be inhibited if the cells were allowed to attach to fibronectin through the alpha5beta1 integrin suggesting that the Bit1-AES pathway contributing to anoikis is regulated by integrins, and in particular, the alpha5beta1 integrin.
Alternate Names: Bit1 , Bcl-2 inhibitor of transcription 1 / Peptidyl-tRNA hydrolase 2
Application Notes: E: 1:500-1:1,000; WB: 1:100-1:500; ICC: 1:100-1:500
Accession No.: NP_057161
Antigen: KLH-conjugated synthetic peptide encompassing a sequence within human BIT1.
Format: Each vial contains 0.1 ml IgG in PBS pH 7.4 with 0.02% sodium azide. Antibody was purified by immunogen affinity chromatography.
Storage:
Store at -20°C. Minimize freeze-thaw cycles. Product is guaranteed one year from the date of shipment.
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