Anti-FANCI antibody (ab15344)
- Datasheet
- References (8)
- Protocols
Overview
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Product nameAnti-FANCI antibody
See all FANCI primary antibodies -
DescriptionRabbit polyclonal to FANCI
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Host speciesRabbit
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Tested applicationsSuitable for: ICC/IF, IP, WBmore details
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Species reactivityReacts with: Human
Predicted to work with: Chimpanzee, Rhesus monkey, Gorilla, Orangutan -
Immunogen
Synthetic peptide within Human FANCI aa 200-250. The exact sequence is proprietary.
Database link: Q9NVI1 -
Positive control
- WB: HeLa cell nuclear extract. ICC/IF: HeLa cells.
Properties
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FormLiquid
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C. Avoid freeze / thaw cycle.
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Storage bufferPreservative: 0.09% Sodium azide
Constituent: Tris citrate/phosphate
pH 7 to 8 -
Concentration information loading...
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PurityImmunogen affinity purified
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ClonalityPolyclonal
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IsotypeIgG
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Research areas
Associated products
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Compatible Secondaries
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Isotype control
Applications
Our Abpromise guarantee covers the use of ab15344 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 | Use at an assay dependent concentration. PubMed: 19465922 | |
IP | Use at 1-4 µg/mg of lysate. | |
WB | 1/2500 - 1/10000. Detects a band of approximately 145 kDa (predicted molecular weight: 149, 142, 27 kDa). |
Target
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FunctionRequired for maintenance of chromosomal stability. Involved in the repair of DNA double-strand breaks by homologous recombination and in the repair of DNA cross-links. Participates in S phase and G2 phase checkpoint activation upon DNA damage. Promotes FANCD2 ubiquitination and recruitment to DNA repair sites.
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Involvement in diseaseDefects in FANCI are a cause of Fanconi anemia complementation group I (FANCI) [MIM:609053]. It is a disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.
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DomainThe C-terminal 30 residues are probably required for function in DNA repair.
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Post-translational
modificationsMonoubiquitinated on Lys-523 during S phase and upon genotoxic stress. Deubiquitinated by USP1 as cells enter G2/M, or once DNA repair is completed. Monoubiquitination requires the FANCA-FANCB-FANCC-FANCE-FANCF-FANCG-FANCM complex. Ubiquitination is required for binding to chromatin, DNA repair, and normal cell cycle progression.
Phosphorylated in response to DNA damage by ATM and/or ATR. -
Cellular localizationNucleus. Concentrates in nuclear foci upon genotoxic stress.
- Information by UniProt
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Database links
- Entrez Gene: 55215 Human
- Omim: 611360 Human
- SwissProt: Q9NVI1 Human
- Unigene: 513126 Human
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Alternative names
- FANCI antibody
- FANCI gene antibody
- FANCI_HUMAN antibody
see all
Images
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Immunocytochemistry/ Immunofluorescence - Anti-FANCI antibody (ab15344)Image courtesy of an Abreview submitted by Dr. Kirk McManus, Univ. of Manitoba/Cancer Care MICB, Canadaab15344 (1/400) staining FANCI in HeLa cells (green). Cells were fixed in paraformaldehyde, permeabilized with 0.5% Triton X-100/PBS and counterstained with DAPI in order to highlight the nucleus (red). for further experimental details please refer to Abreview.
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All lanes : Anti-FANCI antibody (ab15344) at 1/5000 dilution
Lane 1 : HeLa nuclear extract at 5 µg
Lane 2 : HeLa nuclear extract at 20 µg
Developed using the ECL technique.
Predicted band size: 149, 142, 27 kDa
Exposure time: 15 minutes
Protocols
References
This product has been referenced in:
- Jin L et al. MAST1 Drives Cisplatin Resistance in Human Cancers by Rewiring cRaf-Independent MEK Activation. Cancer Cell 34:315-330.e7 (2018). Read more (PubMed: 30033091) »
- Tan SLW et al. A Class of Environmental and Endogenous Toxins Induces BRCA2 Haploinsufficiency and Genome Instability. Cell 169:1105-1118.e15 (2017). Read more (PubMed: 28575672) »