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Explore how neutrophils shape the immune response in health and disease. This poster highlights neutrophil pathogen defense mechanisms, including phagocytosis, degranulation, and NETosis, as well as neutrophil roles in inflammation and NET-associated pathologies.
DOWNLOAD NOWc-Jun N-terminal kinases (JNKs) are stress-activated serine/threonine protein kinases and members of the MAPK family with roles in cell proliferation, differentiation, apoptosis, and migration.1,2 JNKs are encoded by three distinct genes, JNK1, JNK2, and JNK3, which produce 10 variants via alternative splicing. JNK1 and JNK2 are ubiquitously expressed while JNK3 is expressed at high levels in the CNS and low levels in cardiac smooth muscle and the testis.1 In response to stress stimuli, such as osmotic or UV shock, cytokines, or growth factor signaling, JNKs are activated by phosphorylation at threonine 183 (Thr183) and tyrosine 185 (Tyr185) by MKK7 and MKK4, respectively, in a synergistic manner, and induce various transcription factor-mediated downstream signaling events.3,1 Neuronal levels of JNK (phospho- Thr183/Tyr185) are increased in mouse models of sporadic and prion-induced Alzheimer's disease.4 Renal JNK (phospho- Thr183/Tyr185) levels are increased in patients with glomerulonephritis and diabetic neuropathy and are associated with the degree of glomerulosclerosis and macrophage infiltration.2 Cayman's JNK1/2/3 (Phospho-Thr183/Tyr185) Rabbit Monoclonal Antibody (Clone RM464) can be used for immunohistochemistry (IHC) and Western blot (WB) applications.
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1. JNK pathway signaling: A novel and smarter therapeutic target for various biological diseases. Future Med. Chem. 7(15), 2065-2086 (2015).
2. The JNK signaling pathway in renal fibrosis. Front. Physiol. 8(829), (2017).
3. Activation by phosphorylation and purification of human c-
4. The JNK/c-