| Chronic intermittent hypoxia-induced oxidative stress activates TRB3 and phosphorylated JNK to mediate insulin resistance and cell apoptosis in the pancreas. | Chronic intermittent hypoxia-induced oxidative stress activates TRB3 and phosphorylated JNK to mediate insulin resistance and cell apoptosis in the pancreas.
Zeng S, Wang Y, Ai L, Huang L, Liu Z, He C, Bai Q, Li Y. | 02/12/2024 |
| MAPK8 and CAPN1 as potential biomarkers of intervertebral disc degeneration overlapping immune infiltration, autophagy, and ceRNA. | MAPK8 and CAPN1 as potential biomarkers of intervertebral disc degeneration overlapping immune infiltration, autophagy, and ceRNA.
Zhang Y, Zhang J, Sun Z, Wang H, Ning R, Xu L, Zhao Y, Yang K, Xi X, Tian J., Free PMC Article | 06/24/2023 |
| Anti-high-mobility group box-1 (HMGB1) mediates the apoptosis of alveolar epithelial cells (AEC) by receptor of advanced glycation end-products (RAGE)/c-Jun N-terminal kinase (JNK) pathway in the rats of crush injuries. | Anti-high-mobility group box-1 (HMGB1) mediates the apoptosis of alveolar epithelial cells (AEC) by receptor of advanced glycation end-products (RAGE)/c-Jun N-terminal kinase (JNK) pathway in the rats of crush injuries.
Zhang BF, Song W, Wang J, Wen PF, Zhang YM., Free PMC Article | 04/2/2022 |
| FGF21 impedes peripheral myelin development by stimulating p38 MAPK/c-Jun axis. | FGF21 impedes peripheral myelin development by stimulating p38 MAPK/c-Jun axis.
Zhang Y, Jiang K, Xie G, Ding J, Peng S, Liu X, Sun C, Tang X. | 09/11/2021 |
| Isoform-specific functions of c-Jun N-terminal kinase 1 and 2 in lung ischemia-reperfusion injury through the c-Jun/activator protein-1 pathway. | Isoform-specific functions of c-Jun N-terminal kinase 1 and 2 in lung ischemia-reperfusion injury through the c-Jun/activator protein-1 pathway.
Tan J, Gao W, Yang W, Zeng X, Wang L, Cui X. | 08/7/2021 |
| JUN Amino-Terminal Kinase 1 Signaling in the Proximal Tubule Causes Cell Death and Acute Renal Failure in Rat and Mouse Models of Renal Ischemia/Reperfusion Injury. | JUN Amino-Terminal Kinase 1 Signaling in the Proximal Tubule Causes Cell Death and Acute Renal Failure in Rat and Mouse Models of Renal Ischemia/Reperfusion Injury.
Grynberg K, Ozols E, Mulley WR, Davis RJ, Flavell RA, Nikolic-Paterson DJ, Ma FY. | 05/22/2021 |
| Chrysophanol Protects Against Acute Heart Failure by Inhibiting JNK1/2 Pathway in Rats. | Chrysophanol Protects Against Acute Heart Failure by Inhibiting JNK1/2 Pathway in Rats.
Xie XJ, Li CQ., Free PMC Article | 05/22/2021 |
| c-Jun N-terminal kinase (JNK)-dependent internalization and Rab5-dependent endocytic sorting mediate long-distance retrograde neuronal death induced by axonal BDNF-p75 signaling. | c-Jun N-terminal kinase (JNK)-dependent internalization and Rab5-dependent endocytic sorting mediate long-distance retrograde neuronal death induced by axonal BDNF-p75 signaling.
Escudero CA, Cabeza C, Moya-Alvarado G, Maloney MT, Flores CM, Wu C, Court FA, Mobley WC, Bronfman FC., Free PMC Article | 10/24/2020 |
| Long noncoding RNA MALAT-1 inhibits apoptosis and matrix metabolism disorder in interleukin-1beta-induced inflammation in articular chondrocytes via the JNK signaling pathway. | Long noncoding RNA MALAT-1 inhibits apoptosis and matrix metabolism disorder in interleukin-1β-induced inflammation in articular chondrocytes via the JNK signaling pathway.
Gao GC, Cheng XG, Wei QQ, Chen WC, Huang WZ. | 09/19/2020 |
| FBXW5 reduction alleviates spinal cord injury by blocking microglia activity and down-regulating p38 and JNK. | FBXW5 reduction alleviates spinal cord injury (SCI) by blocking microglia activity: A mechanism involving p38 and JNK.
Zhao P, Chao W, Li W. | 06/20/2020 |
| JNK1 expression is elevated in liver cells of rats of different lines receiving excess of easily digested carbohydrates. | Comparative Analysis of JNK1 Expression in Liver Cells in Rats of Different Lines Receiving Excess of Easily Digested Carbohydrates: Confocal Microscopy.
Semin MO, Apryatin SA, Gmoshinskii IV, Nikityuk DB. | 04/4/2020 |
| It was demonstrated in the present study that Syk was markedly activated in the development of Diabetic cardiomyopathy, subsequently promoting NLRP3 inflammasome activation through the phosphorylation of JNK, leading to the cleavage of pro-caspase-1 and maturation of IL-1beta, and finally contributing to diabetic cardiac dysfunction. | Spleen tyrosine kinase‑induced JNK‑dependent NLRP3 activation is involved in diabetic cardiomyopathy.
Li S, Liu R, Xue M, Qiao Y, Chen Y, Long G, Tian X, Hu Y, Zhou P, Dong X, Qi Z, Cui Y, Shen Y. | 08/24/2019 |
| This study suggests that hypothyroidism could affect male reproductive function by disturbing expression of AR, changing the activity of Ca(2+)-ATPase, inducing oxidative stress and then leading to activation of p38MAPK and JNK signaling in the testicular mitochondria. | Influence of hypothyroidism on testicular mitochondrial oxidative stress by activating the p38 mitogen-activated protein kinase and c-Jun NH(2)-terminal kinase signaling pathways in rats.
Chang XR, Yao YL, Wang D, Ma HT, Gou PH, Li CY, Wang JL. | 03/30/2019 |
| Autophagy protects bone marrow mesenchymal stem cells from palmitate-induced apoptosis through the reactive oxygen speciesJNK/p38 MAPK signaling pathways. | Autophagy protects bone marrow mesenchymal stem cells from palmitate‑induced apoptosis through the ROS‑JNK/p38 MAPK signaling pathways.
Liu Y, Wang N, Zhang S, Liang Q., Free PMC Article | 11/3/2018 |
| The JNK signaling pathway is involved in regulating trypsinogen activation in rat pancreatic AR42J cells. SP600125 is an ATPcompetitive, efficient, selective and reversible inhibitor of JNK. the results were verified by four sets of experiments and demonstrated that trypsinogen activation is mediated by the JNK signaling pathway in the pathogenesis of acute pancreatitis | Role of the c-Jun N-terminal kinase signaling pathway in the activation of trypsinogen in rat pancreatic acinar cells.
Yang Z, Yang W, Lu M, Li Z, Qiao X, Sun B, Zhang W, Xue D. | 07/21/2018 |
| the dual inhibition of JNK and p38 led to maximal amelioration of lung IRI in the PMVECs of the IRI model of LT, which occurred through antiinflammatory, antioxidative and antiapoptotic mechanisms. | Amelioration of lung ischemia‑reperfusion injury by JNK and p38 small interfering RNAs in rat pulmonary microvascular endothelial cells in an ischemia‑reperfusion injury lung transplantation model.
Wang J, Tan J, Liu Y, Song L, Li D, Cui X. | 07/7/2018 |
| These findings suggest anti-inflammatory roles of CTGF-stimulated tendon stem cells that are likely associated with improved tendon healing. | Tendon stem/progenitor cells regulate inflammation in tendon healing via JNK and STAT3 signaling.
Tarafder S, Chen E, Jun Y, Kao K, Sim KH, Back J, Lee FY, Lee CH., Free PMC Article | 10/14/2017 |
| this study suggests a link between melatonin, JNK, FoxO1 and IDO1 that acts as a potential balance regulator of tryptophan metabolism, and offers a new approach to treat diseases related to dysregulation of tryptophan metabolism | Regulating the balance between the kynurenine and serotonin pathways of tryptophan metabolism.
Li Y, Hu N, Yang D, Oxenkrug G, Yang Q. | 07/8/2017 |
| Ischemia/reperfusion-induced JNK phosphorylation was reduced by SP600125, indicating that JNK mediates the apoptosis pathways in rat skin. | Inhibition of c-Jun N-terminal kinase signaling suppresses skin flap apoptosis in a rat ischemia and/or reperfusion model.
Bai M, Liu Y, Yin D, Zhang M, Wang Y, Ma X, Liu Y, Zhao P. | 07/8/2017 |
| In summary, our results suggest that HO-1 can decrease H/R-induced myocardiac cell apoptosis; the mechanism may be related to the activation of the Akt signaling pathway and, furthermore, to the inhibition of the JNK/c-Jun/caspase-3 signaling pathway. | Heme oxygenase 1 induction protects myocardiac cells against hypoxia/reoxygenation-induced apoptosis : The role of JNK/c-Jun/Caspase-3 inhibition and Akt signaling enhancement.
Li C, Zhang C, Wang T, Xuan J, Su C, Wang Y. | 06/24/2017 |
| The activation of JNK and p38 MAPK pathways in OGD-treated PC12 cells was suppressed by exogenous Act A and enhanced by ActRIIA-Ab. Together, our results suggest that Act A/Smads signaling pathway negatively regulates OGD-induced autophagy via suppression of JNK and p38 MAPK pathways in neuronal PC12 cells. | CHOP deficiency inhibits methylglyoxal-induced endothelial dysfunction.
Choi YY, Kim S, Han JH, Nam DH, Park KM, Kim SY, Woo CH. | 06/3/2017 |
| Data indicate that mitogen activated protein kinases c-Jun N-terminal kinase, p38, and ERK1/2 were activated but with different distributing patterns in the placenta. | Mitogen-Activated Protein Kinases Are Activated in Placental Injury in Rat Model of Acute Pancreatitis in Pregnancy.
Zuo T, Yu J, Wang WX, Zhao KL, Chen C, Deng WH, He XB, Wang P, Shi Q, Guo WY. | 04/1/2017 |
| The effects of RNA interference-mediated GLT1 gene silencing on cell viability, JNK activation, NMDAR (NR1 and NR2B) activation, cell apoptosis and Akt activation in the hippocampal neuronal cells were slightly reversed by propofol treatment. | Propofol protects hippocampal neurons from apoptosis in ischemic brain injury by increasing GLT-1 expression and inhibiting the activation of NMDAR via the JNK/Akt signaling pathway.
Gong HY, Zheng F, Zhang C, Chen XY, Liu JJ, Yue XQ. | 03/25/2017 |
| Data show that ischemia-reperfusion (I/R) significantly increased the phosphorylation of JNK and p38 kinases and mitochondrial permeability transition (MPT) opening, while these effects were partly abolished by morphine postconditioning (MpostC). | Morphine Postconditioning Protects against Reperfusion Injury via Inhibiting JNK/p38 MAPK and Mitochondrial Permeability Transition Pores Signaling Pathways.
Chen Z, Zhang X, Liu Y, Liu Z. | 02/18/2017 |
| JNK1 activation plays a role in the biological link between depression and NASH. Sitagliptin significantly decreased expression of hepatic JNK1 in rat model of NAFLD with mild chronic stress. | Potential involvement of JNK1 repression in the hepatic effect of sitagliptin and metformin in rats subjected to high fat diet and chronic mild distress.
Magdy YM, El-Kharashi OA, Nabih ES, Shaker SM, Abd-Elaziz LF, Aboul-Fotouh S. | 02/18/2017 |