AmoyDx JAK2 Mutation Detection Kit
- Known as:
- AmoyDx JAK2 Mutation Detection Kit
- Catalog number:
- ADx-JA01
- Product Quantity:
- 24 Kit size (test/kit)
- Category:
- -
- Supplier:
- GENTA
- Gene target:
- AmoyDx JAK2 Mutation Detection Kit
Related genes to: AmoyDx JAK2 Mutation Detection Kit
- Gene:
- JAK2 NIH gene
- Name:
- Janus kinase 2
- Previous symbol:
- -
- Synonyms:
- JTK10
- Chromosome:
- 9p24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-04-16
- Date modifiied:
- 2019-04-23
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- The intratumoural mycobiome is a critical constituent of the tumour microenvironment; however, its specific impact on epithelial ovarian cancer (EOC) progression and the underlying molecular mechanisms remain largely elusive. In this study, internal transcribed spacer 1 (ITS1) sequencing revealed a significant enrichment of Malassezia in EOC tissues compared with epithelial borderline ovarian tumours, with its abundance positively correlated with disease progression. Subsequent intratumoural microbiota transplantation and mono-colonisation in a murine EOC model demonstrated that Malassezia restricta substantially accelerated tumour growth and increased M2 macrophage infiltration. Furthermore, in vitro assays established that M. restricta-derived extracellular vesicles (MrEVs) play a pivotal role in inducing M2 macrophage polarisation. Mechanistically, both in vitro and in vivo data showed that MrEVs activate the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signalling pathway, thereby driving M2 polarisation and tumour malignancy. Collectively, these findings identify M. restricta as a pro-tumourigenic fungus in EOC and uncover a previously unrecognised fungal-immune axis that promotes tumour progression. This study provides new insight into the oncogenic role of tumour-resident fungi and highlights the M. restricta EV-JAK2/STAT3 axis as a potential therapeutic target for immune modulation. - Source: PubMed
Jiang YingWei FenYang QinglingWu XueHuang QifaDai AngChen QiChen Tingtao - Diabetes mellitus is a chronic metabolic disorder in which persistent hyperglycemia promotes oxidative stress, inflammatory activation, and progressive liver injury. Alpha‑lipoic acid (ALA) is an endogenous and diet‑derived antioxidant with glucose‑lowering and insulin‑sensitizing actions. Still, its therapeutic efficacy is constrained by low oral bioavailability and rapid metabolism. In this context, the present study compared the hepatic pharmacodynamic effects of free ALA and ALA‑loaded chitosan nanoparticles (ALA‑CNPs) in streptozotocin (STZ)‑induced diabetic rats. Here, pharmacodynamic effects refer to the biochemical and molecular actions on hepatic tissue, including modulation of oxidative stress markers, activation of cytoprotective signaling pathways such as Nrf2/HO‑1, and inhibition of pro‑inflammatory cascades (e.g., TLR4/NF‑κB and JAK2/STAT1), which collectively contribute to hepatoprotection. Diabetes was induced by a single intraperitoneal injection of STZ (60 mg/kg). Rats with fasting blood glucose ≥ 250 mg/dL were randomized into six groups (n = 15/group): non‑diabetic control, non‑diabetic + ALA, non‑diabetic + ALA‑CNPs, untreated diabetic, diabetic + ALA, and diabetic + ALA‑CNPs. Treatments were administered once daily for 4 weeks. STZ‑induced diabetes caused marked hyperglycemia, reduced serum insulin, dyslipidemia, increased serum alanine and aspartate aminotransferase activities, enhanced hepatic malondialdehyde, depletion of superoxide dismutase, catalase, glutathione peroxidase, and reduced glutathione, and downregulation of the Nrf2/HO‑1 pathway. These changes were accompanied by elevated hepatic tumor necrosis factor‑α, interleukin‑6, and interleukin‑1β; activation of Toll‑like receptor‑4/nuclear factor‑κB and Janus kinase‑2/signal transducer and activator of transcription‑1 signaling, and hepatocellular necrosis; vacuolation; mitochondrial swelling; and endoplasmic reticulum disorganization. Both ALA and ALA‑CNPs attenuated these metabolic, biochemical, and structural disturbances, but ALA‑CNPs produced more pronounced reductions in fasting blood glucose and improvements in lipid profile, antioxidant status, and liver histology. ALA‑CNPs also more effectively upregulated Nrf2/HO‑1 and suppressed Toll‑like receptor‑4/nuclear factor‑κB and Janus kinase‑2/signal transducer and activator of transcription‑1 activation and pro‑inflammatory cytokines. These findings indicate that nano‑encapsulation of ALA enhances its hepatoprotective pharmacological profile in diabetes‑associated liver injury by concomitantly targeting oxidative stress and inflammatory signaling cascades. - Source: PubMed
Publication date: 2026/06/06
Abdalla Hussein AbdelazizElmorsy Ekramy MJawad Najlaa M MHosny NoraShams Ahmed SAyaz Rawan AhmedFawzy Manal SElshopakey Gehad E - Pulmonary fibrosis (PF) is a progressive interstitial lung disease with accumulation of extracellular matrix. Interleukin-6 (IL-6) levels are elevated in PF-associated chronic inflammatory conditions. This study investigated the roles of janus kinase 2 (JAK2), signal transducer and activator of transcription 3 (STAT3), and p300 in IL-6-induced expression of connective tissue growth factor (CTGF) in human lung fibroblasts. IL-6 time- and concentration-dependently induced CTGF expression. JAK2 dominant negative mutant (DN) or STAT3 DN transfection downregulated IL-6-induced CTGF expression. IL-6 time-dependently induced JAK2 and STAT3 phosphorylation. JAK2 DN transfection reduced STAT3 phosphorylation and STAT3-luciferase activity. p300 knockdown inhibited IL-6-induced CTGF expression. IL-6 time-dependently induced p300 phosphorylation, which was blocked by JAK2 DN transfection. IL-6 induced STAT3 acetylation, which was attenuated by JAK2 DN transfection and p300 knockdown. p300 knockdown inhibited IL-6-induced STAT3-luciferase activity. IL-6 promoted the formation of a p300-STAT3 complex, which was recruited to the CTGF promoter region. Expression of CTGF, JAK2, STAT3, and p300 and activation of JAK2, STAT3, and p300 were higher in primary lung fibroblasts from idiopathic pulmonary fibrosis (IPF) patients than from normal subjects; these levels were markedly reduced by IL-6 receptor knockdown. In conclusion, IL-6 induces the activation of STAT3 and p300 through a JAK2-dependent mechanism, leading to the formation of a p300-STAT3 complex, which is recruited to the CTGF promoter region and ultimately triggers CTGF expression in human lung fibroblasts. Overall, IL-6 regulates not only the expression of CTGF, JAK2, STAT3, and p300 but also the activation of JAK2, STAT3, and p300 in primary lung fibroblasts from patients with IPF. - Source: PubMed
Publication date: 2026/06/04
Lee Hong-ShengTsai Jui-YiHua Hung-ShengHsu Hsao-HsunChen Bing-ChangLin Chien-Huang - Acute liver injury (ALI) is a severe liver disease induced by various factors, including hepatitis viruses and drug toxicity. Severe and persistent ALI can eventually progress to multiple organ failure in the absence of effective intervention. At present, existing treatments for liver injury fail to provide effective and safe long-term management. Therefore, it is urgent to develop new anti-liver injury drugs. - Source: PubMed
Publication date: 2026/05/27
Zhang QinqinDai HaoyangCui TianyiChen Suiqing - Retinitis pigmentosa (RP) is a hereditary retinal disorder distinguished by progressive photoreceptor cell (PRC) loss, in which glial activation can accelerate degeneration. Diosgenin, a natural steroidal sapogenin with potent anti-inflammatory properties, has shown therapeutic potential for ocular and neurodegenerative diseases but has not been explored for retinal degeneration. This study examined the protective role of diosgenin against PRC degeneration and explored potential anti-inflammatory mechanisms in an N-methyl-N-nitrosourea (MNU)-induced mouse model of retinal degeneration. - Source: PubMed
Tong WanqingCao JinfengZhou XuebinJia BoLi DanFu Jinling