c_Jun (Phospho_Thr93) Antibody
- Known as:
- c_Jun (Phospho_Thr93) Antibody
- Catalog number:
- E011022-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- c_Jun (Phospho_Thr93) Antibody
Related products to: c_Jun (Phospho_Thr93) Antibody
Related articles to: c_Jun (Phospho_Thr93) Antibody
- IL-11, a novel target for drug development, has been associated with several fibroinflammatory diseases including thyroid eye disease (TED), where it plays an important role in signaling to stromal cells activating multiple intracellular pathways. In TED patient tissue, IL-11 is elevated and stimulates multiple effects important in disease progression, including the production of proinflammatory cytokines, hyaluronic acid (HA) and fibrotic markers. LASN01, a potent antibody to IL-11 receptor, inhibits these effects and is a potential therapeutic agent for TED. Teprotumumab, an antibody to IGF-1 receptor, inhibits HA production and adipogenesis and is effective in reduction of proptosis. Activation of the IGF-1 and IL-11 pathways in TED tissue induces the expression of fibroinflammatory genes regulated by LASN01 and lipid biosynthetic genes regulated by Teprotumumab. Clinical studies show that LASN01 is well tolerated and in a placebo-controlled phase II trial in TED, LASN01 resulted in a statistically significant resolution of clinical activity score (CAS) in 88% of treated patients (p = 0.028), but had lesser effects on proptosis. The data supports the importance of IL-11 biology in fibroinflammatory disease and that IL-11 receptor is a pharmacologically active target for drug development. - Source: PubMed
Publication date: 2026/05/02
King David JSwaney James SRich CadmusJun H ToniVasquez YasminGeller ShiraChidester ChristineChai MerrickElliott EricWitherden DeborahHershoff HannahKafi AaryaStrauwald AmyKossler Andrea LSilkiss Rona ZOester AlanGarrido-Hermosilla Antonio MMalik MohsanKikkawa Don OFardis Maria - Skin photoaging is predominantly induced by ultraviolet (UV) irradiation. Intense pulsed light (IPL) is a commonly employed non-ablative treatment for photoaging. However, the effects and mechanisms of IPL on UV-induced skin photoaging remain insufficiently understood. In this study, we aimed to examine the anti-photoaging effects of IPL and elucidate the underlying mechanisms. This study revealed that UV triggered extracellular signal-regulated kinases (ERK) together with c-jun NH2-terminal kinase (JNK), while selectively suppressed UV-induced ERK phosphorylation while activating JNK in human skin keratinocytes. The different ERK/JNK expression patterns induced by UV and IPL resulted in distinct c-fos/c-jun (activator protein 1) phosphorylation, cyclin D1 expression, and matrix metalloproteinase (MMP) secretion. In vivo, IPL inhibited MMP expression in guinea pig skin and promoted c-fos/c-jun phosphorylation, epidermal proliferation, and collagen remodeling. These findings indicated that ERK was involved in IPL rejuvenation by regulating c-fos, c-jun, cyclin D1, and MMPs, providing a potential target for skin rejuvenation. - Source: PubMed
Publication date: 2026/05/02
Liu CongcongHu WenzhiZhang XiaoyangLu MingminXiang JiayiTan LinaTao YeMa KuiZhang LixiaYang ZhaotingGu Weijie - The c-Jun N-terminal kinase (JNK) pathway is an evolutionarily conserved signaling cascade that regulates development, stress responses, and pathogenesis. While aberrant JNK activation is linked to cancer and neurodegeneration, its regulatory mechanisms are not fully understood. Here, we identify the RNA-binding protein Ataxin-2 (Atx2) as a novel, essential regulator of JNK-mediated cell death and migration in Drosophila. Atx2 deficiency suppressed JNK-dependent apoptosis, tumor growth and invasion, and thorax closure in normal development, while its overexpression activated JNK signaling, promoting cell death, migration, and tissue remodeling. Mechanistically, Atx2 binds the 3' UTR of hipk mRNA, stabilizing it to enhance the expression of Hipk, a core upstream JNK kinase. Strikingly, this mechanism is conserved: human ATXN2L potently activated Hipk-JNK signaling and cell death in Drosophila and HeLa cells. Our findings reveal a conserved post-transcriptional mechanism for JNK pathway regulation and nominate Atx2 family proteins as potential therapeutic targets in JNK-associated pathologies. - Source: PubMed
Publication date: 2026/05/02
Li XinyaoZhu XiaojieLi WenzheDeng HansongXue Lei - - Source: PubMed
Publication date: 2026/03/06
Young Steven KOsman Brian M - - Source: PubMed
Fleisher Lee A