Anti-PKC alpha PRKCA Rabbit Monoclonal Antibody

Overview

This product is an anti-PRKCA antibody for target detection and characterization. Key identifiers include host species: Rabbit; Monoclonal; clone CHO-16; isotype Rabbit IgG; reactivity: Human,Mouse,Rat. Reported application contexts include WB, IHC, ICC, IF, IP, Flow (as provided in the source record). Boster Bio Anti-PKC alpha PRKCA Rabbit Monoclonal Antibody catalog # M00743. Tested in WB, IHC, ICC/IF, IP, Flow Cytometry applications. This antibody reacts with Human, Mouse, Rat.

Key elements and design rationale

• Target: PRKCA (Protein kinase C alpha type).
• Antibody format: Monoclonal; clone CHO-16; isotype Rabbit IgG.
• Host: Rabbit.
• Species reactivity: Human,Mouse,Rat (confirm in your model system with appropriate controls).

This description is intended to help interpret the antibody design and the biological context of the target using the fields provided in the catalog record, alongside general experimental considerations.

Biological background

PRKCA (protein: T-cell surface glycoprotein CD4) is a commonly studied target in molecular and cellular biology. Functional context (as provided): Calcium-activated, phospholipid- and diacylglycerol (DAG)-dependent serine/threonine-protein kinase that is involved in positive and negative regulation of cell proliferation, apoptosis, differentiation, migration and adhesion, tumorigenesis, cardiac hypertrophy, angiogenesis, platelet function and inflammation, by ly phosphorylating targets such as RAF1, BCL2, CSPG4, TNNT2/CTNT, or activating signaling cascade involving MAPK1/3 (ERK1/2) and RAP1GAP. Involved in cell proliferation and cell growth arrest by positive and negative regulation of the cell cycle. Can promote cell growth by phosphorylating and activating RAF1, which mediates the activation of the MAPK/ERK signaling cascade, and/or by up-regulating CDKN1A, which facilitates active cyclin-dependent kinase (CDK) complex formation in glioma cells. In intestinal cells stimulated by the phorbol ester PMA, can trigger a cell cycle arrest program which is associated with the accumulation of the hyper-phosphorylated growth-suppressive form of RB1 and induction of the CDK inhibitors CDKN1A and CDKN1B. Exhibits anti-apoptotic function in glioma cells and protects them from apoptosis by suppressing the p53/TP53-mediated activation of IGFBP3, and in leukemia cells mediates anti-apoptotic action by phosphorylating BCL2. During macrophage differentiation induced by macrophage colony-stimulating factor (CSF1), is translocated to the nucleus and is associated with macrophage development. After wounding, translocates from focal contacts to lamellipodia and participates in the modulation of desmosomal adhesion. Plays a role in cell motility by phosphorylating CSPG4, which induces association of CSPG4 with extensive lamellipodia at the cell periphery and polarization of the cell accompanied by increases in cell motility. Is highly expressed in a number of cancer cells where it can act as a tumor promoter and is implicated in malignant phenotypes of several tumors such as gliomas and breast cancers. Negatively regulates myocardial contractility and positively regulates angiogenesis, platelet aggregation and thrombus formation in arteries. Mediates hypertrophic growth of neonatal cardiomyocytes, in part through a MAPK1/3 (ERK1/2)- dependent signaling pathway, and upon PMA treatment, is required to induce cardiomyocyte hypertrophy up to heart failure and death, by increasing protein synthesis, protein-DNA ratio and cell surface area. Regulates cardiomyocyte function by phosphorylating cardiac troponin T (TNNT2/CTNT), which induces significant reduction in actomyosin ATPase activity, myofilament calcium sensitivity and myocardial contractility. In angiogenesis, is required for full endothelial cell migration, adhesion to vitronectin (VTN), and vascular endothelial growth factor A (VEGFA)-dependent regulation of kinase activation and vascular tube formation. Involved in the stabilization of VEGFA mRNA at post-transcriptional level and mediates VEGFA-induced cell proliferation. In the regulation of calcium-induced platelet aggregation, mediates signals from the CD36/GP4 receptor for granule release, and activates the integrin heterodimer ITGA2B- ITGB3 through the RAP1GAP pathway for adhesion. During response to lipopolysaccharides (LPS), may regulate selective LPS-induced macrophage functions involved in host defense and inflammation. But in some inflammatory responses, may negatively regulate NF- kappa-B-induced genes, through IL1A-dependent induction of NF- kappa-B inhibitor alpha (NFKBIA/IKBA). Upon stimulation with 12-O- tetradecanoylphorbol-13-acetate (TPA), phosphorylates EIF4G1, which modulates EIF4G1 binding to MKNK1 and may be involved in the regulation of EIF4E phosphorylation. Phosphorylates KIT, leading to inhibition of KIT activity. Phosphorylates ATF2 which promotes cooperation between ATF2 and JUN, activating transcription. . Reported cellular localization context: Cytoplasm. Cell membrane; Peripheral membrane protein. Mitochondrion membrane ; Peripheral membrane protein . Nucleus. Tissue expression notes (as provided): Ubiquitous. Expressed at high levels in testis.

Research relevance and current trends

• Research context keywords from the source record include: Cancer,Cardiovascular,Hypertrophy,Protein Phosphorylation,Ser/Thr Kinases,Serine/Threonine Kinases,Signal Transduction.
• Current studies often focus on connecting target abundance/localization to pathway perturbations across models, tissues, and cell states.
• Quantitative and multiplexed assays (e.g., imaging + immunoblot panels) are commonly used to compare phenotypes across conditions and time-courses.

Common research applications

• Western blotting (WB): assess relative target abundance across samples, treatments, or time-points.
• Immunohistochemistry (IHC): evaluate spatial distribution of target-positive staining in tissue architecture.
• Immunofluorescence/ICC (IF/ICC): visualize subcellular localization patterns and cell-to-cell heterogeneity.
• Flow cytometry: quantify target-positive populations and compare shifts in marker distributions.
• Immunoprecipitation (IP): enrich target complexes for downstream immunoblot or interaction analyses.

Workflow ideas (metafield): Validate PRKCA antibody specificity using KO/KD control samples (WB/IF/IHC as appropriate), Detect PRKCA expression by Western blot in cell or tissue lysates, Detect PRKCA in FFPE tissue sections by immunohistochemistry, Localize PRKCA by immunofluorescence/immunocytochemistry in cultured cells, Quantify PRKCA-positive cells by flow cytometry in single-cell suspensions, Enrich PRKCA by immunoprecipitation from lysates for downstream analysis

Notes for experimental interpretation

• Consider isoforms and post-translational modifications (PTMs) that may shift apparent molecular weight or epitope accessibility.
• Apparent molecular weight may vary by sample type and processing (observed MW: 133 kDa; calculated MW: 76750 MW).
• Control concepts: include appropriate negative controls (e.g., isotype, KO/KD samples) and orthogonal validation when feasible.

Additional product details (from the source record)

• Molecular weight (observed): 133 kDa
• Cellular localization (provided): Cytoplasm. Cell membrane; Peripheral membrane protein. Mitochondrion membrane ; Peripheral membrane protein . Nucleus.
• Tissue details (provided): Ubiquitous. Expressed at high levels in testis.

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.