The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Protein concentration is above or equal to 0.05 mg/ml. Best use within three months from the date of receipt of this protein.
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Shipped on dry ice. Upon delivery aliquot and store at -80ºC. Avoid freeze / thaw cycles.
pH: 8.00 Constituents: 0.79% Tris HCl, 0.3% Glutathione
HCF C-terminal chain 6
Host cell factor
Host cell factor 1
Host cell factor C1
Host cell factor C1 (VP16 accessory protein)
VP16 accessory protein
Involved in control of the cell cycle. Also antagonizes transactivation by ZBTB17 and GABP2; represses ZBTB17 activation of the p15(INK4b) promoter and inhibits its ability to recruit p300. Coactivator for EGR2 and GABP2. Tethers the chromatin modifying Set1/Ash2 histone H3 'Lys-4' methyltransferase (H3K4me) and Sin3 histone deacetylase (HDAC) complexes (involved in the activation and repression of transcription, respectively) together. In case of human herpes simplex virus (HSV) infection, HCFC1 forms a multiprotein-DNA complex with the viral transactivator protein VP16 and POU2F1 thereby enabling the transcription of the viral immediate early genes.
Highly expressed in fetal tissues and the adult kidney. Present in all tissues tested.
Contains 5 Kelch repeats.
The HCF repeat is a highly specific proteolytic cleavage signal. The kelch repeats fold into a 6-bladed kelch beta-propeller called the beta-propeller domain which mediates interaction with HCFC1R1.
Proteolytically cleaved at one or several PPCE--THET sites within the HCF repeats. Further cleavage of the primary N- and C-terminal chains results in a 'trimming' and accumulation of the smaller chains. O-glycosylated. Ubiquitinated. Lys-1807 and Lys-1808 are ubiquitinated both via 'Lys-48'- and 'Lys-63'-linked polyubiquitin chains. BAP1 mediated deubiquitination of 'Lys-48'-linked polyubiquitin chains; deubiquitination by BAP1 does not seem to stabilize the protein.
Cytoplasm. Nucleus. HCFC1R1 modulates its subcellular localization and overexpression of HCFC1R1 leads to accumulation of HCFC1 in the cytoplasm. Nuclear in general, but uniquely cytoplasmic in trigeminal ganglia, becoming nuclear upon HSV reactivation from the latent state.