Anti-PKC gamma/PRKCG Antibody Picoband®

Overview

This antibody is intended for detection of PRKCG in biological samples using common immunoassay formats. It is typically selected based on target identity, species reactivity, clonality/clone information, and detection modality.

Vendor notes: Boster Bio Anti-PKC gamma/PRKCG Antibody Picoband® catalog # A01890. Tested in ICC/IF, IHC, WB applications. This antibody reacts with Human, Mouse, Rat. The brand Picoband indicates this is a premium antibody that guarantees superior quality, high affinity, and strong signals with minimal background in Western blot applications. Only our best-performing antibodies are designated as Picoband, ensuring unmatched performance.

Key elements and design rationale

• Antibody format: Rabbit Polyclonal Rabbit IgG
• Immunogen / epitope context: A synthetic peptide corresponding to a sequence at the C-terminus of human PKC gamma/PRKCG, identical to the related mouse and rat sequences.
• Molecular weight context: reported MW: 78 kDa; calculated MW: 146424 MW
• Reactivity: Human,Mouse,Rat
• Applications: ICC/IF, IHC, WB

As a polyclonal antibody, the reagent recognizes multiple epitopes on the target, which can improve detection robustness but may increase sensitivity to sample-dependent epitope changes.

Biological background

protein kinase C, gamma. The gamma isotype of protein kinase C (PKC gamma) is a member of the classical PKC (cPKC) subfamily which is activated by Ca (2+) and diacylglycerol in the presence of phosphatidylserine. Physiologically, PKC gamma is activated by a mechanism coupled with receptor-mediated breakdown of inositol phospholipid as other cPKC isotypes such as PKC alpha and PKC beta. PKC gamma is expressed solely in the brain and spinal cord and its localization is restricted to neurons, while PKC alpha and PKC beta are expressed in many tissues in addition to the brain. Within the brain, PKC gamma is the most abundant in the cerebellum, hippocampus and cerebral cortex, where the existence of neuronal plasticity has been demonstrated. PKC gamma gene is mutated in spinocerebellar ataxia type 14 (SCA14). Verbeek et al. (2005) point out the specific alterations in mutant PKC gamma function that could lead to the selective neuronal degeneration of SCA14. Functional note: Calcium-activated, phospholipid- and diacylglycerol (DAG)-dependent serine/threonine-protein kinase that plays diverse roles in neuronal cells and eye tissues, such as regulation of the neuronal receptors GRIA4/GLUR4 and GRIN1/NMDAR1, modulation of receptors and neuronal functions related to sensitivity to opiates, pain and alcohol, mediation of synaptic function and cell survival after ischemia, and inhibition of gap junction activity after oxidative stress. Binds and phosphorylates GRIA4/GLUR4 glutamate receptor and regulates its function by increasing plasma membrane-associated GRIA4 expression. In primary cerebellar neurons treated with the agonist 3,5-dihyidroxyphenylglycine, functions downstream of the metabotropic glutamate receptor GRM5/MGLUR5 and phosphorylates GRIN1/NMDAR1 receptor which plays a key role in synaptic plasticity, synaptogenesis, excitotoxicity, memory acquisition and learning. May be involved in the regulation of hippocampal long-term potentiation (LTP), but may be not necessary for the process of synaptic plasticity. May be involved in desensitization of mu-type opioid receptor-mediated G-protein activation in the spinal cord, and may be critical for the development and/or maintenance of morphine-induced reinforcing effects in the limbic forebrain. May modulate the functionality of mu-type-opioid receptors by participating in a signaling pathway which leads to the phosphorylation and degradation of opioid receptors. May also contributes to chronic morphine-induced changes in nociceptive processing. Plays a role in neuropathic pain mechanisms and contributes to the maintenance of the allodynia pain produced by peripheral inflammation. Plays an important role in initial sensitivity and tolerance to ethanol, by mediating the behavioral effects of ethanol as well as the effects of this drug on the GABA (A) receptors. During and after cerebral ischemia modulate neurotransmission and cell survival in synaptic membranes, and is involved in insulin-induced inhibition of necrosis, an important mechanism for minimizing ischemic injury. Required for the elimination of multiple climbing fibers during innervation of Purkinje cells in developing cerebellum. Is activated in lens epithelial cells upon hydrogen peroxide treatment, and phosphorylates connexin-43 (GJA1/CX43), resulting in disassembly of GJA1 gap junction plaques and inhibition of gap junction activity which could provide a protective effect against oxidative stress (By similarity). Phosphorylates p53/TP53 and promotes p53/TP53-dependent apoptosis in response to DNA damage. Involved in the phase resetting of the cerebral cortex circadian clock during temporally restricted feeding. Stabilizes the core clock component ARNTL/BMAL1 by interfering with its ubiquitination, thus suppressing its degradation, resulting in phase resetting of the cerebral cortex clock. Reported localization: Cell membrane. Peripheral membrane protein. Cytoplasm. perinuclear region. Synaptosome. Dendrite. Expression/tissue context: Expressed in Purkinje cells of the cerebellar cortex.

Research relevance and current trends

• Cancer: Researchers commonly examine how PRKCG relates to this theme using model systems and orthogonal readouts.
• Cardiovascular: Researchers commonly examine how PRKCG relates to this theme using model systems and orthogonal readouts.
• Hypertrophy: Researchers commonly examine how PRKCG relates to this theme using model systems and orthogonal readouts.

Common research applications

• Western blotting: compare relative PRKCG levels across conditions; band patterns may reflect isoforms and processing.
• IHC/IHC-F: assess spatial distribution of PRKCG across tissue regions and cell types using matched controls.

Notes for experimental interpretation

• Specificity notes: No cross reactivity with other proteins.
• Cross-reactivity: No cross-reactivity with other proteins.
• Isoforms and PTMs: Apparent size and signal patterns can differ across splice isoforms, proteolytic processing, and post-translational modifications.
• Controls: Include an isotype control (as relevant), no-primary control for imaging, and orthogonal validation such as KD/KO samples when available.

Customization & Add-ons: Can’t find the antibody you need—or require a custom format for your assay? We can help you source the best match or support custom antibody solutions for diverse research needs, including species and isotype selection, conjugations and labeling (e.g., HRP/AP, biotin, fluorophores), purification grade options (Protein A/G, affinity purified), formulation preferences (buffer selection, carrier-free, glycerol-free), custom concentrations and aliquoting, low-endotoxin options for cell-based work, and application-focused QC/validation support (project dependent). Click Talk to a Scientist to submit a request, email us at support@biohippo.com, or explore our Research Services for additional support—our team will follow up with feasibility details and next steps.