Recombinant Ubiquitin HUMAN
- Known as:
- Recombinant Ubiquitin HUMAN
- Catalog number:
- REP0012
- Product Quantity:
- 100ug
- Category:
- -
- Supplier:
- DIATHEVA
- Gene target:
- Recombinant Ubiquitin HUMAN
Related genes to: Recombinant Ubiquitin HUMAN
- Gene:
- JAK3 NIH gene
- Name:
- Janus kinase 3
- Previous symbol:
- -
- Synonyms:
- L-JAK, JAKL, LJAK, JAK3_HUMAN, JAK-3
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-19
- Date modifiied:
- 2019-04-23
Related products to: Recombinant Ubiquitin HUMAN
Related articles to: Recombinant Ubiquitin HUMAN
- The macromolecular monoclonal antibodies targeting CTLA-4/PD-1/PD-L1 have revolutionized cancer immunotherapy. However, their clinical efficacy is limited by poor tissue penetration, strong immunogenicity and frequent cytokine release syndrome (CRS) risk. In contrast, natural small molecules can effectively overcome these challenges due to their strong penetration, minimal immunogenicity and low CRS risk. - Source: PubMed
Publication date: 2026/07/24
Dai ZhiLiu Fu-RaoWang Xin-HuiXia MiaoYang Meng-JiaoZhao Li-XingZhao Yun-LiLuo Xiao-Dong - Alopecia universalis (AU) is a severe autoimmune disorder characterized by complete loss of scalp and body hair. The introduction of Janus kinase (JAK) inhibitors has expanded therapeutic options for patients with severe disease; however, treatment responses remain variable, particularly among individuals with extensive and longstanding hair loss. Reporting cases with atypical or limited responses to therapy remains important for understanding the spectrum of clinical outcomes observed in practice. We describe a 30-year-old man with a 23-year history of AU who demonstrated minimal response to multiple prior therapies, including tofacitinib (pan-JAK inhibitor) and ritlecitinib (JAK3/TEC inhibitor), without meaningful scalp, eyebrow, or eyelash regrowth. Following six months of treatment with deuruxolitinib, the patient experienced his first clinically significant regrowth, limited to the eyebrows and eyelashes, while scalp involvement remained largely unchanged. This case highlights the potential for site-specific hair regrowth in longstanding, treatment-refractory AU and suggests that eyebrow and eyelash regrowth may occur even in the absence of substantial scalp hair recovery. - Source: PubMed
Publication date: 2026/06/29
Kogan SimonaLutwak MoisesLutwak DanielHoward TaraSkopit StanleyBhardwaj Sumeet - : Janus kinase inhibitors (JAK inhibitors) have expanded therapeutic options for rheumatoid arthritis (RA), although factors associated with treatment response in routine clinical practice remain incompletely defined. : This study aimed to evaluate clinical, treatment-related and pharmacogenetic factors associated with response to different JAK inhibitors in patients with RA. : An ambispective observational real-world cohort study was conducted in patients with RA treated with tofacitinib, baricitinib, filgotinib, or upadacitinib. Disease activity was assessed at 3 and 6 months using the Disease Activity Score in 28 joints based on C-reactive protein (DAS28-CRP). Clinical response was evaluated according to European Alliance of Associations for Rheumatology (EULAR) response criteria, low disease activity (LDA), and remission thresholds. Clinical, laboratory, and treatment-related variables were collected, and selected single-nucleotide polymorphisms (SNPs) in , , and genes were genotyped. Bivariate and multivariable analyses were performed to identify variables associated with treatment outcomes. : Lower baseline inflammatory burden and lower disease activity were consistently associated with higher probabilities of EULAR response, LDA, and remission across JAK inhibitors. Treatment-related factors were also associated with improved outcomes. Pharmacogenetic associations were heterogeneous and drug-specific, with the most recurrent exploratory signals involving variants. However, these genetic findings showed variability across outcomes and time points. : In this real-world RA cohort, clinical and treatment-related factors were the most consistent variables associated with response to JAK inhibitors. Pharmacogenetic variation within the JAK pathway, particularly involving , may contribute to drug-specific variability in response, but these findings should be considered exploratory because of the limited sample size, multiple comparisons, and sparse genotype subgroups. Larger independent studies are required before JAK genotyping can be incorporated into individualized treatment strategies. - Source: PubMed
Publication date: 2026/07/11
Roldán Alicia MartínMárquez Pete NoeliaSánchez Suárez María Del MarRojo Tolosa SusanaJiménez Morales Alberto - Bisphenol A (BPA) is a common industrial chemical primarily used in the manufacture of plastics, and it has been found in more than 90% of people worldwide. As an endocrine disruptor, BPA can impair reproduction, development, immunity, metabolism, and cognition; it also disturbs immune balance and thus fosters chronic inflammation. A number of population-based studies have indicated a link between environmental BPA exposure and atopic dermatitis (AD). Nevertheless, the detailed molecular pathways connecting BPA to AD remain poorly understood. AD is the leading chronic recurrent inflammatory skin disorder, characterized by severe itching and repeated eczema-like lesions. Its prevalence is roughly 13% among children and 5% among adults, and its global incidence continues to rise, imposing heavy health and economic burdens on societies. To clarify whether and how BPA may promote or worsen AD, we carried out a comprehensive computational study that integrated network toxicology, transcriptomic data, machine learning, molecular docking, and molecular dynamics simulations. From the CTD, ChEMBL, and SwissTargetPrediction databases, we collected 5701 potential BPA targets; from GeneCards and OMIM, we obtained 3270 genes linked to AD. The overlap between these two gene sets gave a group of common candidate genes. Enrichment analyses using GO and KEGG showed that these common genes were significantly overrepresented in the PI3K-Akt signaling pathway, Th17 cell differentiation, and the JAK-STAT signaling pathway-all central to immune and inflammatory regulation. We then built a protein-protein interaction (PPI) network by submitting the common genes to the STRING database and employed Cytoscape to extract hub genes from that network. By integrating human AD transcriptomic profiles with the hub genes and applying two machine learning techniques (LASSO and SVM), we identified six core toxic targets of BPA in AD: , , , , , and . These six targets fall into two main functional categories: immune dysregulation and inflammatory cell infiltration. Subsequent molecular docking and molecular dynamics simulation experiments confirmed that BPA binds well to all six targets and can form stable complexes with them. Collectively, our findings offer a preliminary experimental foundation for future investigations into the pathogenesis of BPA-induced AD and provide important molecular evidence for understanding how environment-gene interactions contribute to complex inflammatory skin diseases such as AD. - Source: PubMed
Publication date: 2026/06/25
Cao XingxinCai XiangkaiLi MingxueJin WeihuaYang FengmeiDuan SuqinLi YanyanHe Zhanlong - Janus kinase 3 (JAK3) has long been pursued as a potentially safer and more selective therapeutic target because of its predominant expression in hematopoietic cells, its association with common γ-chain cytokine receptors, and the presence of the non-conserved Cys909 residue near the ATP-binding site. This review examines the biological role of JAK3 in hematological malignancies and the medicinal chemistry strategies developed to achieve selective JAK3 inhibition. Particular attention is given to the evolution of covalent and non-covalent inhibitors, structural determinants of selectivity, and the translational challenges associated with JAK3-targeted drug discovery. Collectively, the available evidence suggests that biochemical selectivity alone is insufficient to predict therapeutic benefit, since γc cytokine signaling depends on cooperative JAK1/JAK3 activity. Covalent targeting of Cys909 has provided the most successful route to high intra-JAK selectivity and sustained target engagement, whereas non-covalent inhibitors continue to face challenges arising from ATP-site conservation. Current evidence further indicates that the therapeutic potential of JAK3 inhibition is most compelling in molecularly defined hematological malignancies with demonstrable JAK3 pathway dependence. Overall, the available literature supports the view that the clinical relevance of JAK3 inhibition depends not only on kinase selectivity but also on biological context, functional pathway dependence, and disease-specific molecular characteristics. - Source: PubMed
Publication date: 2026/07/25
Dias SaraParise-Filho Roberto