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HIC1 Rabbit pAb
HIC1 Rabbit pAb
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Application 
| WB |
|---|---|
| Primary Accession | Q14526 |
| Reactivity | Mouse |
| Predicted | Human, Rat, Chicken, Dog, Pig, Horse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 76508 Da |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from human HIC1 |
| Epitope Specificity | 501-650/733 |
| Isotype | IgG |
| Purity | affinity purified by Protein A |
| Buffer | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| SUBCELLULAR LOCATION | Nucleus. |
| SIMILARITY | Belongs to the krueppel C2H2-type zinc-finger protein family. Hic subfamily.Contains 1 BTB (POZ) domain.Contains 5 C2H2-type zinc fingers. |
| SUBUNIT | Self-associates. Interacts with HIC2. Interacts with CTBP1 and CTBP2. Interacts with TCF7L2 and ARID1A. Interacts with MTA1 and MBD3; indicative for an association with the NuRD complex. |
| Post-translational modifications | Acetylated on several residues, including Lys-333. Lys-333 is deacetylated by SIRT1.Sumoylated on Lys-333 by a PIAS family member, which enhances interaction with MTA1, positively regulates transcriptional repression activity and is enhanced by HDAC4. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | 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. |
| Gene ID | 3090 |
|---|---|
| Other Names | Hypermethylated in cancer 1 protein, Hic-1, Zinc finger and BTB domain-containing protein 29, HIC1, ZBTB29 |
| Target/Specificity | Ubiquitously expressed with highest levels found in lung, colon, prostate, thymus, testis and ovary. Expression is absent or decreased in many tumor cells. |
| Dilution | WB=1:500-2000 |
| Storage | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
| Name | HIC1 |
|---|---|
| Synonyms | ZBTB29 |
| Function | Transcriptional repressor (PubMed:12052894, PubMed:15231840). Recognizes and binds to the consensus sequence '5- [CG]NG[CG]GGGCA[CA]CC-3' (PubMed:15231840). May act as a tumor suppressor (PubMed:20154726). Involved in development of head, face, limbs and ventral body wall (By similarity). Involved in down- regulation of SIRT1 and thereby is involved in regulation of p53/TP53- dependent apoptotic DNA-damage responses (PubMed:16269335). The specific target gene promoter association seems to be depend on corepressors, such as CTBP1 or CTBP2 and MTA1 (PubMed:12052894, PubMed:20547755). In cooperation with MTA1 (indicative for an association with the NuRD complex) represses transcription from CCND1/cyclin-D1 and CDKN1C/p57Kip2 specifically in quiescent cells (PubMed:20547755). Involved in regulation of the Wnt signaling pathway probably by association with TCF7L2 and preventing TCF7L2 and CTNNB1 association with promoters of TCF-responsive genes (PubMed:16724116). Seems to repress transcription from E2F1 and ATOH1 which involves ARID1A, indicative for the participation of a distinct SWI/SNF-type chromatin-remodeling complex (PubMed:18347096, PubMed:19486893). Probably represses transcription of ACKR3, FGFBP1 and EFNA1 (PubMed:16690027, PubMed:19525223, PubMed:20154726). |
| Cellular Location | Nucleus. |
| Tissue Location | Ubiquitously expressed with highest levels found in lung, colon, prostate, thymus, testis and ovary. Expression is absent or decreased in many tumor cells |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
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.
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