Anti-KAP1 (phospho S824) antibody (ab84077)
Key features and details
- Rabbit polyclonal to KAP1 (phospho S824)
- Suitable for: ICC/IF
- Reacts with: Human
- Isotype: IgG
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Overview
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Product name
Anti-KAP1 (phospho S824) antibody
See all KAP1 primary antibodies -
Description
Rabbit polyclonal to KAP1 (phospho S824) -
Host species
Rabbit -
Tested applications
Suitable for: ICC/IFmore details -
Species reactivity
Reacts with: Human
Predicted to work with: Chimpanzee, Rhesus monkey, Gorilla, Orangutan -
Immunogen
Synthetic peptide corresponding to Human KAP1 (phospho S824).
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Positive control
- Neocarzinostatin treated asynchronous HeLa cells. Untreated asynchronous HeLa cells.
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General notes
Concentration is optimized for IHC and not determined
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Properties
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Form
Liquid -
Storage instructions
Shipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles. -
Storage buffer
pH: 6.8
Preservative: 0.09% Sodium azide
Constituents: 0.1% BSA, Tris buffered saline -
Concentration information loading...
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Purity
Immunogen affinity purified -
Clonality
Polyclonal -
Isotype
IgG -
Research areas
Associated products
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Compatible Secondaries
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Isotype control
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Recombinant Protein
Applications
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab84077 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Application | Abreviews | Notes |
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ICC/IF |
Notes |
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Likely to work with frozen sections.
Not yet tested in other applications.
Optimal dilutions/concentrations should be determined by the end user.
Target
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Function
Nuclear corepressor for KRAB domain-containing zinc finger proteins (KRAB-ZFPs). Mediates gene silencing by recruiting CHD3, a subunit of the nucleosome remodeling and deacetylation (NuRD) complex, and SETDB1 (which specifically methylates histone H3 at 'Lys-9' (H3K9me)) to the promoter regions of KRAB target genes. Enhances transcriptional repression by coordinating the increase in H3K9me, the decrease in histone H3 'Lys-9 and 'Lys-14' acetylation (H3K9ac and H3K14ac, respectively) and the disposition of HP1 proteins to silence gene expression. Recruitment of SETDB1 induces heterochromatinization. May play a role as a coactivator for CEBPB and NR3C1 in the transcriptional activation of ORM1. Also corepressor for ERBB4. Inhibits E2F1 activity by stimulating E2F1-HDAC1 complex formation and inhibiting E2F1 acetylation. May serve as a partial backup to prevent E2F1-mediated apoptosis in the absence of RB1. Important regulator of CDKN1A/p21(CIP1). Has E3 SUMO-protein ligase activity toward itself via its PHD-type zinc finger. -
Tissue specificity
Expressed in all tissues tested including spleen, thymus, prostate, testis, ovary, small intestine, colon and peripheral blood leukocytes. -
Pathway
Protein modification; protein sumoylation. -
Sequence similarities
Belongs to the TRIM/RBCC family.
Contains 2 B box-type zinc fingers.
Contains 1 bromo domain.
Contains 1 PHD-type zinc finger.
Contains 1 RING-type zinc finger. -
Domain
The HP1 box is both necessary and sufficient for HP1 binding.
The PHD-type zinc finger enhances CEBPB transcriptional activity. The PHD-type zinc finger, the HP1 box and the bromo domain, function together to assemble the machinery required for repression of KRAB domain-containing proteins. Acts as an intramolecular SUMO E3 ligase for autosumoylation of bromodomain.
The RING-finger-B Box-coiled-coil/tripartite motif (RBCC/TRIM motif) is required for interaction with the KRAB domain of KRAB-zinc finger proteins. Binds four zinc ions per molecule. The RING finger and the N-terminal of the leucine zipper alpha helical coiled-coil region of RBCC are required for oligomerization.
Contains one Pro-Xaa-Val-Xaa-Leu (PxVxL) motif, which is required for interaction with chromoshadow domains. This motif requires additional residues -7, -6, +4 and +5 of the central Val which contact the chromoshadow domain. -
Post-translational
modificationsPhosphorylated upon DNA damage, probably by ATM or ATR. ATM-induced phosphorylation on Ser-824 represses sumoylation leading to the de-repression of expression of a subset of genes involved in cell cycle control and apoptosis in response to genotoxic stress. Dephosphorylation by the phosphatases, PPP1CA and PP1CB forms, allows sumoylation and expression of TRIM28 target genes.
Sumoylation/desumoylation events regulate TRIM28-mediated transcriptional repression. Sumoylation is required for interaction with CHD3 and SETDB1 and the corepressor activity. Represses and is repressed by Ser-824 phosphorylation. Enhances the TRIM28 corepressor activity, inhibiting transcriptional activity of a number of genes including GADD45A and CDKN1A/p21. Lys-554, Lys-779 and Lys-804 are the major sites of sumoylation. In response to Dox-induced DNA damage, enhanced phosphorylation on Ser-824 prevents sumoylation and allows de-repression of CDKN1A/p21. -
Cellular localization
Nucleus. Associated with centromeric heterochromatin during cell differentiation through CBX1. - Information by UniProt
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Database links
- Entrez Gene: 10155 Human
- Entrez Gene: 711982 Rhesus monkey
- Omim: 601742 Human
- SwissProt: Q13263 Human
- Unigene: 467408 Human
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Alternative names
- E3 SUMO protein ligase TRIM28 antibody
- E3 SUMO-protein ligase TRIM28 antibody
- FLJ29029 antibody
see all
Images
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ab84077 at 1/250 dilution staining KIP1 in Neocarzinostatin treated asynchronous HeLa cells by Immunocytochemistry / Immunofluorescence. A FITC conjugated anti rabbit used at a dilution of 1/100 as secondary.
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Detection of Human Phospho KAP1 (S824) by Immunocytochemistry.
Samples: Untreated asynchronous HeLa cells (formaldehyde fixation).Antibody: ab84077 used at a dilution of 1/250.
Detection: Anti-rabbit IgG-FITC conjugated used at a dilution of 1/100.
Protocols
Datasheets and documents
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SDS download
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Datasheet download
References (2)
ab84077 has been referenced in 2 publications.
- Parmar K et al. The CHK1 Inhibitor Prexasertib Exhibits Monotherapy Activity in High-Grade Serous Ovarian Cancer Models and Sensitizes to PARP Inhibition. Clin Cancer Res 25:6127-6140 (2019). PubMed: 31409614
- Biddlestone-Thorpe L et al. ATM kinase inhibition preferentially sensitizes p53-mutant glioma to ionizing radiation. Clin Cancer Res 19:3189-200 (2013). PubMed: 23620409