JNK1
- Known as:
- JNK1
- Catalog number:
- 000085A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- JNK1
Related genes to: JNK1
- Gene:
- MAPK8 NIH gene
- Name:
- mitogen-activated protein kinase 8
- Previous symbol:
- PRKM8
- Synonyms:
- JNK, JNK1, SAPK1
- Chromosome:
- 10q11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-28
- Date modifiied:
- 2016-10-05
Related products to: JNK1
Related articles to: JNK1
- Lung ischemia-reperfusion injury (LIRI) is a principal cause of primary graft dysfunction (PGD) following lung transplantation, severely compromising recipient survival. However, effective therapies remain unavailable due to its complex pathophysiology. Pterostilbene (PTE) is a natural stilbene compound known for its well-documented anti-inflammatory, antioxidant, and antitumor properties. However, its effects and underlying mechanisms in LIRI remain unclear. - Source: PubMed
Publication date: 2026/04/01
Bai HaotianZhao HengFeng JintengWang HongyiLi YixingChen ZheHe BinWang ChiGao RuiZhao RuiGao ShanZhang Guangjian - : The objective of the study was to investigate the mRNA expression of critical gene patterns, including IL-6, CCL2, IL-10, MAPK1, MAPK8, MMP9, COL1A1, COL3A1, and TGFB1, and their associations with adverse postoperative outcomes in reconstructive and plastic surgery patients, depending on age. : A total of 95 women participated in this prospective longitudinal cohort study and underwent reconstructive/plastic surgery. The mean age was 35.48 ± 6.61 years (range: 19-57). mRNA expression of IL-6, CCL2, IL-10, MAPK1, MAPK8, MMP9, COL1A1, COL3A1, and TGFB1 genes was evaluated in peripheral blood leukocytes using a PCR-based method with reverse transcription of cDNA. : The risk of postoperative complications significantly increased with elevated expression levels of IL-6 and COL3A1 (7.5-fold, = 0.007), CCL2 (6.2-fold, = 0.012), and MAPK1 (25.5-fold, < 0.001). Increased expression of MAPK8, IL-10, and MMP9 was associated with a 13.2-fold higher risk ( < 0.001). The strongest association was observed for COL1A1 overexpression, which increased complication risk by 58.33-fold ( < 0.001). Risk stratification using the Molecular Complication Risk Index (MCRI), incorporating weighted gene contributions, identified an unfavorable molecular profile predominantly among women aged ≥ 40 years. Receiver operating characteristic analysis confirmed the model's discriminative ability (AUC = 0.78; 95% CI 0.68-0.87), with an optimal cut-off value of MCRI ≥ 8.5 (sensitivity 76%, specificity 71%, < 0.05). : The transcriptional activity of IL-6, CCL2, IL-10, MAPK1, MAPK8, MMP9, COL1A1, COL3A1, and TGFB1 is associated with postoperative wound healing risk. Women aged over 40 years are at the highest risk of complications. Implementation of the MCRI model may enable early identification of high-risk patients, support targeted preventive strategies, and improve personalized surgical planning. - Source: PubMed
Publication date: 2026/04/07
Sydorchuk LarysaGumennyi RuslanSydorchuk AndriiBatih IrynaVasiuk ValentinaSydorchuk RuslanKamyshna IrynaPetakh PavloHalabitska IrynaKamyshnyi Oleksandr - Intervertebral disc degeneration (IVDD) is a major cause of chronic low back pain and disability worldwide. Growing evidence highlights oxidative stress as a key driver of disc degeneration; however, the integrated relationships between gene expression, regulatory microRNAs (miRNAs), and protein-level changes across disease stages remain insufficiently understood. This study aimed to identify oxidative stress-related molecular signatures in IVDD and to explore their miRNA-mediated regulation across degeneration grades.The study included 200 patients with lumbosacral IVDD undergoing microdiscectomy and 100 postmortem control samples without spinal pathology. Degeneration severity was classified using the Pfirrmann scale, and pain intensity was assessed with the Visual Analog Scale (VAS). Gene expression of oxidative stress markers was evaluated using RT-qPCR, while protein levels were quantified by ELISA. Additionally, bioinformatic prediction and RT-qPCR validation were used to analyze mRNA-miRNA interactions.Gene expression analysis revealed progressive downregulation of antioxidant genes CAT (FC ≈ -6.40) and GPX1 (FC ≈ -9.56), alongside upregulation of MAPK8 (FC ≈ 8.18) and IL6 (FC ≈ 8.18), with a moderate increase in NRF1 expression. These values reflect comparisons between advanced degeneration (G5) and controls. In contrast, protein analysis showed an inverse trend, with increasing levels of CAT, GPX1, and NRF1 and decreasing levels of MAPK8 and IL6 as degeneration progressed.miRNA profiling demonstrated significant dysregulation, including downregulation of miR-3163 and miR-196a-1-3p and upregulation of miR-665-3p and miR-4686. Correlation analysis indicated that molecular alterations were more strongly associated with structural degeneration than with pain intensity, as VAS-related differences were generally weak and non-significant.Overall, the results reveal a complex regulatory network in IVDD, characterized by discordant mRNA-protein expression and significant miRNA involvement. Oxidative stress and inflammatory pathways appear tightly regulated at transcriptional and post-transcriptional levels and are more closely linked to structural degeneration than clinical pain. - Source: PubMed
Publication date: 2026/04/09
Strojny DamianSzwej KarolStaszkiewcz RafałSobański DawidGogol PawełLehotska MariaMajchrowicz BozenaGrabarek Beniamin Oskar - Methionine sulfoxide reductase B2 (MsrB2), a mitochondrial redox enzyme essential for maintaining protein integrity under oxidative stress, has been implicated in diabetic cardiac remodeling. However, its contribution to hypertension-induced fibrosis remains unclear. Hypertension frequently coexists with diabetes and accelerates cardiac fibrotic remodeling, particularly in non-obese diabetic patients who may exhibit distinct metabolic and oxidative responses. - Source: PubMed
Publication date: 2026/03/12
Yun Ji HoCho SuyeonLee Jong YoulKim SujiLee Seung Hee - - Source: PubMed
Publication date: 2026/03/23
Liu HongxueWang Haidong