Description:

Size: 100ul

Catalog no.: bs-15485R-A488

Price: 380 EUR

Product details

Gene ID Number

3090

Target Antigen

HIC1

Modification Site

None

Tested applications

IF(IHC-P)

French translation

anticorps

Clonality

Polyclonal

Modification

Unmodified

Conjugation

Alexa Fluor

Concentration

1ug per 1ul

Excitation emission

499nm/519nm

Conjugated with

ALEXA FLUOR® 488

Crossreactivity

Human, Mouse, Rat

Clone

Polyclonal antibody

Recommended dilutions

IF(IHC-P)(1:50-200)

Purification

Purified by Protein A.

Category

Conjugated Primary Antibodies

Also known as

Anti-HIC1 PAb ALEXA FLUOR 488

Host Organism

Rabbit (Oryctolagus cuniculus)

Specificity

This is a highly specific antibody against HIC1.

Long name

HIC1 Polyclonal Antibody, ALEXA FLUOR 488 Conjugated

Cross-reactive species details

Due to limited amount of testing and knowledge, not every possible cross-reactivity is known.

Source

This antibody was obtained by immunization of the host with KLH conjugated synthetic peptide derived from human HIC1

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.

Storage conditions

Store this antibody in aqueous buffered solution containing 1% BSA, 50% glycerol and 0.09% sodium azide. Keep refrigerated at 2 to 8 degrees Celcius for up to one year.

Properties

For facs or microscopy Alexa 1 conjugate.Alexa Fluor 488 has the same range to that of fluorescein isothiocyanate (FITC), yet the Anti-HIC1 has a very high photo stability. As a result of this photo stability, it has turned into an antibody for fluorescent microscopy and FACS FLOW cytometry. It is distinguished in the FL1 of a FACS-Calibur or FACScan. Also Alexa Fluor 488 is pH stable.If you buy Antibodies supplied by Bioss Primary Conjugated Antibodies. ALEXA FLUOR they should be stored frozen at - 24°C for long term storage and for short term at + 5°C.

Background of the antigen

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.