Product Name: HIC1 Polyclonal Antibody, FITC Conjugated
Applications: IF(IHC-P)
Reactivity: Human, Mouse, Rat
Conjugation: FITC
Host: Rabbit
Sourcr: KLH conjugated synthetic peptide derived from human HIC1
Clonality: Polyclonal
CAS NO: 289656-45-7
VE-822
Isotype: IgG
Concentration: 1ug/ul
Purification: Purified by Protein A.
Storage: Aqueous buffered solution containing 1% BSA, 50% glycerol and 0.09% sodium azide. Store at 4°C for 12 months.
Synonyms: 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.
Background: 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.
PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/20538607?dopt=Abstract
