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HIC1 Polyclonal Antibody, PE Conjugated

Applications

  • WB

Reactivity

  • Mouse

Predicted Reactivity

  • Human
  • Rat
  • Dog
  • Cow
  • Pig
  • Horse
  • Chicken
Overview
Catalog # bs-15485R-PE
Product Name HIC1 Polyclonal Antibody, PE Conjugated
Applications WB
Reactivity Mouse
Predicted Reactivity Human, Rat, Dog, Cow, Pig, Horse, Chicken
Specifications
Conjugation PE
Host Rabbit
Source KLH conjugated synthetic peptide derived from human HIC1
Immunogen Range 501-650/733
Clonality Polyclonal
Isotype IgG
Concentration 1ug/ul
Purification Purified by Protein A.
Storage Buffer Aqueous buffered solution containing 0.01M TBS (pH 7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
Storage Condition Store at -20°C. Aliquot into multiple vials to avoid repeated freeze-thaw cycles.
Target
Gene ID 3090
Subcellular location Nucleus
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.
Application Dilution
WB 1:300-5000