research use only
Cat.No.: F6483
| Dilution |
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|
| Application |
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| IHC, IF, FCM |
| Reactivity |
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| Human, Mouse, Rat |
| Source |
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| Rabbit Monoclonal Antibody |
| Storage Buffer |
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| PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3 |
| Storage (from the date of receipt) |
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| -20°C (avoid freeze-thaw cycles), 2 years |
| Predicted MW |
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| 77 kDa |
| Specificity |
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| PKC β Antibody [C22A12] detects endogenous levels of total PKC β protein. |
| Clone |
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| C22A12 |
| Synonym(s) |
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| Protein kinase C beta type, PKC-B, PKC-beta, PRKCB, PKCB, PRKCB1 |
| Background |
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| PKC β is a conventional protein kinase C isoform within the serine/threonine kinase family that responds to diacylglycerol and calcium and participates in signaling cascades controlling cell growth, survival, differentiation, cytoskeletal dynamics, and secretory responses. The enzyme contains an N‑terminal regulatory region with C1 domains that bind diacylglycerol and phorbol esters and a C2 domain that senses calcium and anionic phospholipids, plus a C‑terminal catalytic domain that phosphorylates substrates on serine and threonine residues once the autoinhibitory pseudosubstrate segment is released at membranes enriched in acidic phospholipids. Activation of PKC β1 follows receptor‑triggered phospholipase C–dependent generation of diacylglycerol and calcium mobilization, leading to its translocation from the cytosol to the plasma membrane and other membrane compartments, where it phosphorylates target proteins involved in cytoskeletal remodeling, ion transport, gene expression, and metabolism. PKC β1 participates in growth factor signaling; epidermal growth factor activation of PKC β1 promotes reorganization of the F‑actin cytoskeleton, maintenance of barrier cytoarchitecture, and normalization of intracellular calcium by enhancing calcium efflux, linking this isoform to cytoskeletal protection and calcium homeostasis during oxidative or inflammatory stress. PKC β1 also contributes to the regulation of transporters and channels at specialized barriers, including the blood–brain barrier, where pharmacologic activation of PKC β1 modulates P‑glycoprotein activity and alters drug efflux capacity, connecting this kinase to control of central nervous system drug delivery. Within broader signaling networks, PKC β isoforms interface with MAPK/ERK and PI3K/Akt pathways by phosphorylating or regulating upstream and intermediate components, thereby influencing transcription factor activation, cell cycle progression, and survival signaling in immune and non‑immune cells. Elevated PKC β activity associates with vascular dysfunction in metabolic disease, with diacylglycerol‑driven PKC β activation in hyperglycemic conditions contributing to changes in endothelial permeability, extracellular matrix production, and expression of vasoactive mediators that underlie microvascular complications. In lymphoid malignancies, PKC‑β expression is frequently increased, and high PKC‑β levels in diffuse large B‑cell lymphoma correlate with adverse outcome and align with survival pathways that support B‑cell growth and resistance to apoptosis, which has driven interest in PKC β–directed therapeutic strategies. |
| References |
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