Ask about this productRelated genes to: JAK2 antibody
- 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
Related products to: JAK2 antibody
Related articles to: JAK2 antibody
- Polycythemia vera (PV) is a myeloproliferative neoplasm associated with a markedly increased risk of arterial and venous thrombosis. Superior mesenteric artery (SMA) thrombosis is an exceptionally rare but potentially fatal complication. We report the case of a 25-year-old man with previously diagnosed, JAK2-negative PV who presented with acute abdominal pain, nausea, vomiting, abdominal distension, and absence of stool and flatus, consistent with clinical features of intestinal obstruction. Laboratory testing revealed marked leukocytosis, elevated inflammatory markers, and subtherapeutic anticoagulation (INR 1.2) despite ongoing oral therapy. Multislice computed tomography demonstrated occlusion of the SMA with developed collateral circulation and features of small-bowel ischemia. Due to progression to an acute abdomen, emergency laparotomy was performed, revealing jejunal perforation with preserved viability of the remaining bowel. Primary closure was carried out, followed by peritoneal lavage and drainage. The postoperative course was uneventful. After correction of anticoagulation and therapeutic INR monitoring, no recurrent thrombotic events were observed during follow-up. This case underscores the importance of strict anticoagulation control, early imaging, and prompt surgical intervention in patients with PV, even in young individuals and in atypical vascular territories. - Source: PubMed
Publication date: 2026/04/01
Milić LjiljanaArbutina DraganaRadulović RadosavŠurlan MarkoKaramarkovic Aleksandar - Analysis of runs of homozygosity (ROH) in commercial breed genomes is important for accurately assessing the population inbreeding status and exploring homozygous regions related to economic traits formed by selection pressure. The Danish Large White (LW) pig is a commercially important breed renowned for its superior growth efficiency and reproductive performance. In the present study, we identified ROH segments of Danish LW pigs based on 43 individual whole-genome resequencing data. We then calculated the inbreeding coefficient and screened candidate genes with important economic traits from the ROH islands. A total of 9446 ROH segments were identified in the LW pig population. Each LW pig carried 219.67 ROH. Most ROH were , and the average genomic inbreeding coefficient ( ) in LW pigs was 0.24. However, the proportion of ROH ( ) in LW pigs has reached 10 %, indicating selection pressure or inbreeding in recent times. Candidate genes related to reproductive traits (, , , , , , and ), and growth and development traits (, , , , , , , , , , and ) were identified in the genomic ROH islands of LW pigs. In conclusion, the present study provides further assessment of genetic diversity and inbreeding in the Danish LW pig population. In addition, our results provide useful insights into the functions of ROH on a hereditary basis and the role that ROH play in controlling the excellent characteristics of Danish LW pigs. - Source: PubMed
Publication date: 2026/01/12
Ding WeiminWu XudongBu YuZhang WeiWang YuanlangDing YueyunZheng XianruiZhang XiaodongYin Zongjun - Typ515 (W515) mutations in the protein MPL are one of key driver mutations promoting BCR/ABL-negative myeloproliferative neoplasms (MPNs), but their effects on hematopoietic stem cells (HSCs) and MPN-related hematological abnormalities have not been studied in physiological contexts. Here, we established a MplW514L knock-in mouse model which largely mimics human MPLW515L mutation during hematopoiesis. The mutant mice developed an essential thrombocythemia (ET)-like MPN phenotypes, displaying excess megakaryopoiesis and thrombocytosis and progressive myelofibrosis. Mechanistically we observed that MplW514L-conditioned HSC compartment had a unique disease-initiating capacity however it did not exhibit a obvious advantage of competitive repopulation over wild-type control. Notably, single-cell analysis and flow cytometry profiles support that MplW514L expression led to a significant expansion of megakaryocyte-biased stem cell fate within the HSC pool. Finally, JAK2 inhibitor treatment phenotypically alleviated the ET signs but failed to eliminate the disease-initiating HSCs. These findings underscore the etiology of physiological expression of MPLW515L mutation in HSCs, and also provide a valuable in vivo model to evaluate potential therapeutic options for patients with MPLW515L-positive MPN. - Source: PubMed
Publication date: 2026/04/23
Zhang ShujingLiu JingjingLi YuanWang YiWang LinglingXu MiaomiaoLi YanxiaDong GeWang ShanshanLi YanmeiCai ZhigangZhao Baobing - Lung cancer metastasis is the primary cause of patient mortality, underscoring an urgent need for highly effective and low-toxicity therapies. Ursolic acid (UA), a natural triterpenoid, possesses potent antitumor activity, yet its clinical translation has been hindered by poor water solubility, low bioavailability, and nonspecific distribution. To overcome these limitations, we developed a UA-loaded iron-based metal-organic framework (MOF) nanomedicine, termed Ursolic Acid-loaded Iron-MOF (UA@MOF). Harnessing the high surface area and tunable porosity of MOFs, this system enables efficient UA encapsulation and promotes tumor-targeted delivery through the enhanced permeability and retention (EPR) effect. Once internalized, UA suppresses the Janus Kinase 2/Signal Transducer and Activator of Transcription 3 (JAK2/STAT3) signaling pathway, while iron ions released from the MOF induce ferroptosis in tumor cells via Fenton reactions. Together, these dual mechanisms act synergistically to inhibit tumor growth and metastasis. This work presents a novel strategy to improve the delivery and efficacy of natural antitumor agents, offering promising potential for the treatment of metastatic lung cancer. - Source: PubMed
Publication date: 2026/04/22
Wang JiahuiHou WanxinQiu XiuxiuZhang YuTao LiChen YukunHong BeibeiZhou LeiLi HegenZhang Zhanxia - Diabetic nephropathy (DN) is a microvascular disease resulting from diabetes mellitus and is the leading cause of end-stage renal disease worldwide. Recently, ferroptosis, a form of regulated iron-dependent cell death caused by lipid peroxide accumulation, has been suggested to be a major cause of renal tubular injury in diabetics. Concurrently, interleukin-6 (IL-6), a pleiotropic pro-inflammatory cytokine abundantly expressed in the diabetic kidney, has been progressively acknowledged as a key orchestrator of renal pathology. However, the molecular mechanisms by which IL-6 intersects with ferroptotic pathways to drive DN progression remain incompletely defined. In this review, we systematically delineate the molecular circuitry through which IL-6 operates as a key regulator of ferroptosis in the DN. We demonstrate that sustained activation of the the interleukin-6 (IL-6)/Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling axis suppresses critical antioxidant defenses by transcriptionally downregulating glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11), thereby rendering renal cells vulnerable to ferroptotic death. Furthermore, we provide, for the first time, an integrative analysis establishing the causal relationship between IL-6-mediated iron metabolic imbalance and lipid peroxidation in the pathogenesis of DN, revealing how metabolic reprogramming under chronic hyperglycemia amplifies ferroptotic susceptibility through perturbed iron homeostasis. Based on these results, we propose that sustained IL-6 elevation provides a feed-forward loop linking diabetic metabolic stress with ferroptosis injury. We also propose a combination therapy targeting the IL-6-ferroptosis axis with JAK/STAT inhibitors and ferroptosis suppressors, multitarget approaches to overcome single-pathway blockade limitations, and may guide the development of therapies simultaneously targeting inflammation and ferroptosis in DN. - Source: PubMed
Publication date: 2026/04/19
Zhang WenXu SumeiCao ZhijianJin WenDeng ShihuaZhou QiujuXia XiaofanWang Xiaoran