Protein L100 mg
- Known as:
- Protein L100 mg
- Catalog number:
- 6530-100
- Product Quantity:
- 100 mg
- Category:
- -
- Supplier:
- Biovis
- Gene target:
- Protein L100
Ask about this productRelated genes to: Protein L100 mg
- Gene:
- DUSP1 NIH gene
- Name:
- dual specificity phosphatase 1
- Previous symbol:
- PTPN10
- Synonyms:
- HVH1, CL100, MKP-1
- Chromosome:
- 5q35.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-03-03
- Date modifiied:
- 2015-09-11
Related products to: Protein L100 mg
Related articles to: Protein L100 mg
- Effective early prediction of acute pancreatitis (AP) severity remains an unmet clinical need due to limited molecular characterization of systemic immune responses. We performed integrated single-cell RNA sequencing with T- and B-cell receptor profiling on peripheral blood mononuclear cells from AP patients ( = 7) at days 1, 3, and 7 after admission. Immune landscape analysis revealed marked inter-patient heterogeneity, with a distinct expansion of MZB1-expressing plasma cells that were strongly associated with complicated AP and recovery. Functional validation in an independent cohort ( = 14) confirmed disease-associated plasma cell markers, alongside altered serum immunoglobulin and cytokine profiles ( = 32). From these findings, we established a nine-gene B-cell-derived transcriptomic signature (, , , , , , , , and ) predictive of AP severity. This model demonstrated high discriminative performance in internal validation ( = 114; AUROC > 0.95, superior to standard clinical scoring systems), and sustained accuracy in external validation cohorts of AP ( = 87) and AP combined with non-AP sepsis ( = 174) for predicting persistent organ failure. Our study identifies a mechanistic and predictive role for MZB1⁺ plasma cells in AP pathogenesis, offering a novel immune-based stratification strategy with potential for precision clinical management. - Source: PubMed
Publication date: 2025/09/14
Xie RongliXiao GuohuiYang KaigeWang XiaofengChen CongDing MinZhou TongMukherjee RajarshiSutton RobertChen ErzhenChen YingHuang WeiXu DanFei Jian - Lipopolysaccharide (LPS) induces acute lung injury (ALI), a condition characterized by oxidative stress, inflammation, and apoptosis, ultimately leading to respiratory failure. Dual-specificity phosphatase 1 (DUSP1), a key regulator of MAPK signaling, may offer protection against inflammatory damage. - Source: PubMed
Publication date: 2025/08/15
Chen ShengHu YunnanLi LingfengZhang JiaxinHuang RongdaTang Mirong - Renal fibrosis is a hallmark of diabetic kidney disease (DKD), and currently available therapies offer limited efficacy. Artesunate (ART), a repurposed antimalarial agent, has recently demonstrated potential in mitigating renal fibrosis. This study aimed to investigate whether ART protects mitochondrial integrity and attenuates fibrosis in tubular epithelial cells (TECs) via the dual-specificity phosphatase 1 (DUSP1) pathway. Mitochondrial morphology and DUSP1 expression were examined in kidney tissues from DKD patients and db/db mice. ART (25 mg/kg) was administered to db/db mice to evaluate its in vivo effects on fibrosis, mitochondrial dynamics, and inflammation. In vitro, TECs stimulated with high glucose were used to assess mitochondrial function and fibrotic response after ART treatment. Mechanistic studies included RNA sequencing, molecular docking, and genetic modulation (DUSP1 knockdown and overexpression). Mitochondrial swelling, cristae disruption, and TFAM downregulation were observed in both human DKD samples and db/db mice, correlating with tubulointerstitial fibrosis. ART treatment restored mitochondrial structure, reduced fibrotic markers, and suppressed inflammatory cytokines in vivo. In vitro, ART reversed high-glucose-induced mitochondrial dysfunction and fibrotic signaling. Mechanistically, ART directly bound to and stabilized DUSP1, thereby inhibiting MAPK signaling. Knockdown of DUSP1 abolished the protective effects of ART, while DUSP1 overexpression mimicked ART's therapeutic actions. Notably, DUSP1 expression was significantly reduced in DKD patients, associated with greater fibrosis and worse renal function. ART attenuates renal fibrosis and restores mitochondrial homeostasis in DKD through DUSP1 stabilization and MAPK pathway inhibition. These findings support ART as a potential therapeutic agent targeting mitochondrial integrity and inflammation in diabetic kidney disease. - Source: PubMed
Publication date: 2025/09/11
Liu ZikangHu HongtuJin YuxuanBao JiwenZhao HanxueLin YurongDai BinbinPan Yangbin - Cystic fibrosis (CF) is an autosomal recessive disease caused by mutations in the cystic fibrosis transmembrane conductance regulator () gene. CF is characterized by respiratory tract infections, pancreatic insufficiency, meconium ileus, intestinal obstruction, and male infertility. A genotype to phenotype correlation is difficult to establish because of the heterogeneity of disease severity. Even patients with the same mutation can have varying clinical severities. In recent years, studies have explored the role of microRNA (miRNA) expression in the regulation of respiratory diseases. However, no research has been conducted to date on miRNAs in siblings with the same mutation. - Source: PubMed
Publication date: 2025/04/28
Mustafaoğlu AyberkNoyan SenemAkkaya Ulum Yeliz ZGür Dedeoğlu BalaEmiralioğlu NagehanÖzçelik UğurYalçin EbruDoğru DenizKiper NuralDayangaç Erden Didem - The confirmed tumor-inhibitory effects of the 30 kDa Momordica anti-human immunodeficiency virus protein (MAP30) have yet to be complemented by an exploration into its mechanism of action on tumor development and metastasis. For this purpose, we delved into the intrinsic mechanism of MAP30 in bladder cancer (BC). Here, we demonstrated that MAP30 markedly suppressed the proliferation, migration, invasion, and angiogenic capabilities of human BC cells in vitro, and the tumor metastatic potential in vivo. Furthermore, our findings showed that MAP30 suppressed the functional activities of BC cells by upregulating the expression levels of early growth response 1 (EGR1). Additionally, our investigation confirmed that EGR1 and dual specificity phosphatase 1 (DUSP1) were down-expressed in BC and had been identified as closely linked to the advancement of BC. DUSP1 was transcriptionally induced by EGR1, and the expression of EGR1 was found to be positively linked with DUSP1 in human BC tissues. The knockdown of EGR1 was found to boost cell invasion, migration, proliferation, and angiogenesis via the MAPK signaling pathway, however, the overexpression of DUSP1 inhibited EGR1 knockdown-induced promotion of these functional activities in BC cells. Furthermore, MAP30 inhibited the invasion, migration, proliferation, and angiogenesis of BC cells by regulating the EGR1-DUSP1 axis. Our study yielded an exhaustive insight into the suppressive actions of MAP30 on BC progression. - Source: PubMed
Publication date: 2025/09/05
Wang KaiyueGu QiaoXue ChunyanShi JunyuWang KunHe Xiaozhou