Anti-JNK1/JNK3 Rabbit Monoclonal Antibody for WB, IHC-P, IF/ICC, ELISA - P45983 / P53779

Core Product Specifications and Parameters

Biological Background: JNK1/JNK3 Function and Localization

• Mitogen-activated protein kinase 8 (MAPK8), also known as JNK1, is a serine/threonine kinase that acts as a core component of the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway, activated by extracellular stresses and pro-inflammatory cytokines. Related references: PMID:28943315
• Upon activation, JNK1 phosphorylates and regulates AP-1 transcription factors such as JUN, JDP2, and ATF2, thereby controlling gene expression programs involved in cell proliferation, differentiation, and survival. Related references: PMID:18307971
• In response to stress, JNK1 promotes apoptosis by phosphorylating critical regulators like p53/TP53 and Yes-associated protein YAP1, and mediates BAD phosphorylation for erythroid cell survival, as well as starvation-induced BCL2 phosphorylation that triggers autophagy. Related references: PMID:21364637, PMID:21095239, PMID:18570871
• JNK1 phosphorylates the CLOCK-BMAL1 heterodimer, playing a direct role in the regulation of the circadian clock. Related references: PMID:22441692
• A key pro-inflammatory function involves phosphorylation of NLRP3, which promotes assembly of the NLRP3 inflammasome. Related references: PMID:28943315
• Under oxidative stress, JNK1 targets several substrates including EIF4ENIF1 for P-body assembly, SIRT6 to stimulate its mono-ADP-ribosyltransferase activity, and ALKBH5 to enhance its SUMOylation and inactivation. Related references: PMID:22966201, PMID:27568560, PMID:34048572
• JNK1 localizes to the cytoplasm, nucleus, and synapse, and alternative splicing produces multiple isoforms (alpha-1, alpha-2, beta-1, beta-2) with distinct substrate binding properties, fine-tuning downstream signaling events.

Experimental Guidance and Technical Tips

• The immunogen spans the N-terminal region (aa 1–383) of JNK1, which may detect multiple isoforms and both phosphorylated and unphosphorylated forms; however, activation-dependent mobility shifts and the presence of JNK3 cross-reactivity should be considered when interpreting band patterns.
• For Western blot, expect bands around 46–48 kDa, with possible additional lower signals reflecting isoform or degradation products; include appropriate positive and negative controls (e.g., JNK2-expressing vs. JNK2-deficient lysates) to confirm specificity.
• In IHC-P and IF/ICC, standard fixation and antigen retrieval protocols may be applied; however, optimal conditions should be empirically determined for each tissue or cell type, and the absence of cross-reactivity with JNK2 can be leveraged to distinguish JNK1/3-specific localization.
• Since the antibody does not recognize JNK2, it is well-suited for experiments where discrimination between JNK1/3 and JNK2 is required, such as in parallel knockdown or overexpression studies.
• Consider stimulating cells with anisomycin or UV treatment to induce JNK activation and validate the antibody’s ability to detect stress-induced signaling changes.

CamelBio: Your One-Stop Sourcing Bridge

CamelBio provides diagnostic manufacturers, contract research organizations, and academic laboratories with streamlined access to high-quality IVD raw materials, including this JNK1/JNK3 monoclonal antibody. Supporting research in stress signaling, apoptosis, and inflammatory pathways, CamelBio’s portfolio covers validated antibody pairs, optimized monoclonals, bulk ancillary reagents, and custom sourcing for rare targets. By bridging raw material supply with technical and regulatory consulting, CamelBio accelerates your transition from concept to clinic.