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PKC iota, Active recombinant protein
PKC, Protein kinase C iota
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | P41743 |
|---|---|
| Concentration | 0.1 |
| Calculated MW | ~98.0 kDa |
| Gene ID | 5584 |
|---|---|
| Gene Symbol | PRKC1 |
| Other Names | PKC, Protein kinase C iota |
| Source | Baculovirus (Sf9 insect cells) |
| Assay&Purity | SDS-PAGE; ≥90% |
| Assay2&Purity2 | HPLC; |
| Recombinant | Yes |
| Format | Liquid |
| Storage | -80°C; Recombinant protein in storage buffer (50 mM Tris-HCl, pH 7.5, 150 mM NaCl, 0.25 mM DTT, 0.1 mM EGTA, 0.1 mM EDTA, 0.1 mM PMSF, 25% glycerol). |
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Provided below are standard protocols that you may find useful for product applications.
Background
PKC ι is a member of the protein kinase C family of serine-threonine kinases. The amino acid sequence of PKC ι showed greatest homology to PKC zeta, with 72% identity overall rising to 84% in the catalytic domain. In contrast, the homology of PKC ι to the other isoforms is less pronounced, with < 53% identity even in the highly conserved catalytic region. PKC ι transcript is present predominantly in lung and brain, but also expressed at lower levels in many tissues including pancreatic islets. PKC ι is stimulated by tumor necrosis factor α (TNF-α) and is required for the activation of NF-kB by this cytokine. Cell transfections with a PKC ι dominant negative mutant abolished TNF-α-induced NFkB-dependent transcription. PKC ι can modify vulnerability of neural cells to apoptosis induced by amyloid β-peptide (ABP), a cytotoxic peptide linked to neuronal degeneration in Alzheimer's disease. Associated with the increased resistance to apoptosis are improved mitochondrial function and reduced activity of caspases. In addition, ABP-induced increases in levels of oxidative stress and intracellular calcium levels were attenuated in cells overexpressing PKC ι.
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