| Overview |
| bs-15485R-Biotin |
| HIC1 Polyclonal Antibody, Biotin Conjugated |
| WB, ELISA, IHC-P, IHC-F |
| Mouse |
| Human, Rat, Dog, Cow, Pig, Horse, Chicken |
| Specifications |
| Biotin |
| Rabbit |
| KLH conjugated synthetic peptide derived from human HIC1 |
| Polyclonal |
| #REF! |
| IgG |
| 1ug/ul |
| Purified by Protein A. |
| Aqueous buffered solution containing 0.01M TBS (pH 7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| Store at -20C for 12 months. |
| Target |
| 3090 |
| Nucleus |
| Hic 1; Hic-1; Hic1; HIC1_HUMAN; Hypermethylated in cancer 1; Hypermethylated in cancer 1 protein; ZBTB29; Zinc finger and BTB domain-containing protein 29; ZNF901. |
| Hypermethylated in cancer (HIC-1) was originally identified as a target of p53-induced gene expression. HIC-1 is deleted in the genetic disorder Miller-Dieker syndrome (MDS), and the expression of HIC-1 is also frequently suppressed in leukemia and various cancers due to the hypermethylation of specific DNA regions and the resulting transcriptional silencing. These and other studies indicate that HIC-1 acts as a putative tumor suppressor protein that mediates transcriptional repression. HIC-1 is ubiquitously expressed in adult tissues and its structure is defined by five zinc fingers and an N-terminal broad complex POZ (or BTB) domain. In several BTB/POZ containing proteins, including BCL-6 and the promyelocytic leukemia zinc-finger (PLZF) oncoprotein, this domain interacts with the SMRT/N-CoR-mSin3A HDAC complex and is directly involved in repressing and silencing gene transcription. When this domain is deleted, as with the oncogenic PLZF-RAR chimera of promyelocytic leukemias, this transcriptional repression is attenuated. Conversely, HIC-1 does not interact with components of the HDAC complex, suggesting that HIC-1-induced transcriptional repression is unassociated with the POZ/BTB domain. |
| Application Dilution |
| WB |
1:300-5000 |
| ELISA |
1:500-1000 |
| IHC-P |
1:200-400 |
| IHC-F |
1:100-500 |
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