HCFC1 Antibody (Carboxy-terminal Antigen) #50708
Filter:
- WB
- IP
Supporting Data
REACTIVITY | H M R |
SENSITIVITY | Endogenous |
MW (kDa) | 100, 125, 130, 145, 260 |
SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Immunoprecipitation | 1:50 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
HCFC1 Antibody (Carboxy-terminal Antigen) recognizes endogenous levels of total HCFC1 protein. This antibody also recognizes carboxyl terminal fragments (HCFC1-C) resulting from O-GlcNAc transferase (OGT) cleavage.
Species Reactivity:
Human, Mouse, Rat
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Glu1590 of human HCFC1 protein. Antibodies are purified by protein A and peptide affinity chromatography.
Background
Host cell factor C1 (HCFC1) was first identified as the host cell factor for human herpes simplex virus infection. HCFC1 and the viral protein VP16 belong to a multi-protein complex that promotes transcription of viral immediate early genes (1). The relatively large HCFC1 protein contains 6 centrally located 26 amino acid repeats that can be O-GlcNAcylated and subjected to O-linked beta-N-acetylglucosamine transferase (OGT) cleavage (2-4). The resulting amino-terminal (HCFC1-N) and carboxy-terminal (HCFC1-C) fragments are non-covalently associated and play important roles in cell cycle regulation. The HCFC1-N peptide facilitates progression through the G1 phase of the cell cycle while HCFC1-C enables proper mitosis and cytokinesis during the M phase (5-7). As HCFC1 plays an important role in neurodevelopment, mutations in the corresponding gene are associated with neurodevelopmental disorders (e.g., intellectual disability) in humans (8).
- Vogel, J.L. and Kristie, T.M. (2013) Viruses 5, 1272-91.
- Daou, S. et al. (2011) Proc Natl Acad Sci U S A 108, 2747-52.
- Capotosti, F. et al. (2011) Cell 144, 376-88.
- Lazarus, M.B. et al. (2013) Science 342, 1235-9.
- Julien, E. and Herr, W. (2003) EMBO J 22, 2360-9.
- Julien, E. and Herr, W. (2004) Mol Cell 14, 713-25.
- Zargar, Z. and Tyagi, S. (2012) Transcription 3, 187-92.
- Jolly, L.A. et al. (2015) Hum Mol Genet 24, 3335-47.
限制使用
除非 CST 的合法授书代表以书面形式书行明确同意,否书以下条款适用于 CST、其关书方或分书商提供的书品。 任何书充本条款或与本条款不同的客书条款和条件,除非书 CST 的合法授书代表以书面形式书独接受, 否书均被拒书,并且无效。
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For Research Use Only. Not For Use In Diagnostic Procedures.
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