Unconjugated Rabbit anti-Human KAP1 (phospho S824) Monoclonal Antibody [IgG]

Výrobce: Bioss Katalogové č.: bsm-54687R Aplikace: Imunohistochemie, Imunoprecipitace, imunoaglutinace, Ostatní, Western Blot Reaktivita: Human Původ: Rabbit Klonalita: Monoclonal Podtřída: IgG Status: RUO Dodatečné informace: Produkt na webu výrobce Popis:

E3 SUMO protein ligase TRIM28 antibody, E3 SUMO-protein ligase TRIM28 antibody, FLJ29029 antibody, KAP 1 antibody, KAP-1 antibody, KRAB associated protein 1 antibody, KRAB interacting protein 1 antibody, KRAB-associated protein 1 antibody, KRAB-interacting protein 1 antibody, KRIP 1 antibody, KRIP-1 antibody, KRIP1 antibody, Nuclear corepressor KAP 1 antibody, Nuclear corepressor KAP-1 antibody, RING finger protein 96 antibody, RNF96 antibody, TF1B antibody, TIF1 beta antibody, TIF1-beta antibody, TIF1B antibody, TIF1B_HUMAN antibody, Transcription intermediary factor 1 beta antibody, Transcription intermediary factor 1-beta antibody, Trim28 antibody, Tripartite motif containing 28 antibody, tripartite motif containing protein 28 antibody, Tripartite motif-containing protein 28 antibody

The KRAB (Kruppel Associated Box) domain is minimally about 45 amino acids in length and is a transcriptional repression domain found in numerous transcription factors. Over 220 KRAB zinc finger protein (KRAB ZFP) genes have been identified in the human genome. These proteins functionally repress transcription via specific interactions with KAP1 (KRAB Associated Protein 1). KAP1 is an 835 amino acid polypeptide that contains a RING finger, B boxes, and a PHD finger. KAP1 has been shown to form complexes with KRAB domain transcription factors and increase the efficiency with which they mediate repression. KAP1 has also been shown to directly interact with HP1 (heterochromatin protein 1) and KRAZ1 (Kruppel associated box containing zinc finger protein 1). KAP1 directly targets KRAZ1 to the foci of centromeric heterochromatin containing HP1alpha, helping to regulate transcriptional repression. Recent studies have shown that KAP1 mutants with the ability to bind KRAB but unable to bind HP1 leads to random distribution of KRAZ1 and strong transcriptional activation.

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