ALBUMIN HUMAN Recombinant
- Known as:
- ALBUMIN HUMAN Recombinant
- Catalog number:
- 101-10R
- Product Quantity:
- 1 gm
- Category:
- -
- Supplier:
- LeeBio
- Gene target:
- ALBUMIN HUMAN Recombinant
Related genes to: ALBUMIN HUMAN Recombinant
- 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: ALBUMIN HUMAN Recombinant
Related articles to: ALBUMIN HUMAN Recombinant
- Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is caused by impaired central immune tolerance due to deficiency of the Autoimmune Regulator (AIRE) and is characterized by severe, multiorgan autoimmunity. We recently identified interferon-γ (IFN-γ) as a dominant driver of immunopathology in APECED and showed that treatment with the JAK1/2 inhibitor ruxolitinib ameliorates disease in both AIRE-deficient mice and patients. However, broad JAK inhibition is associated with clinically relevant toxicities, raising the question of whether selective targeting of individual JAK pathways can retain efficacy while sparing nonpathogenic immune programs. Here, we systematically evaluated the effects of selective JAK1, JAK2, and JAK3 inhibition in e mice. Selective JAK1 and JAK2 inhibition reduced autoimmune tissue injury, suppressed IFN-γ signaling, and decreased accumulation of pathogenic T cells, with JAK2 inhibition providing the most robust protection, comparable to ruxolitinib. In contrast, selective JAK3 inhibition decreased T cell accumulation, but paradoxically increased the proportion of IFN-γ-producing T cells and did not significantly attenuate IFN-γ-driven tissue inflammation. These findings reveal an unexpected uncoupling between lymphocyte burden and pathogenic cytokine bias and identify IFN-γ signaling as hierarchically dominant over γc-dependent pathways in AIRE deficiency. Together, our data indicate that effective control of APECED-associated autoimmunity requires direct suppression of the IFN-γ-JAK2 axis rather than generalized lymphocyte inhibition and suggest that selective JAK2 targeting may represent a rational strategy to preserve therapeutic efficacy while minimizing disruption of JAK1-and γc-dependent immune functions. - Source: PubMed
Publication date: 2026/03/07
Heller EliezerDos Santos Dias LucasLionakis Michail S - - Source: PubMed
Publication date: 2026/04/29
Rahimi FatemehAbbasi Maryam - Atopic dermatitis (AD) is a heterogeneous inflammatory skin disease with known ethnic disparities in clinical presentation and treatment response. However, molecular data, particularly for Hispanic patients, remain limited. - Source: PubMed
Publication date: 2026/04/25
Liu DanielDel Duca EsterBrunner PatrickAvallone GianlucaBeaziz JessicaMetukuru RagasrutiLin XinyiEstrada YerielLau MeganLargen JosephUngar BenjaminGuttman-Yassky Emma - Extra virgin olive oil (EVOO) is one of the signature foods for cooking and dressing in the Mediterranean diet, and clinical evidence revealed its remarkably lower risk of breast cancer. However, the current anti-tumor constituent studies rarely supported this clinical effect. Thus, it might contain a novel mechanism, and should be clarified. The nontraditional cytotoxicity T-cell immunomodulatory anti-tumor model combination with bioactivity-guided isolation was used to explore its bioactive compound and mechanism. The LDH killing and ELISA analysis were used to examine killing efficacy and cytokines. The mouse breast cancer lung metastasis model was used to evaluate anti-tumor efficacy in vivo through EVOO monotherapy combined with anti-PD-1 treatment. The proteome and phosphoproteome analyses were used to mechanistic study combined with blocking rescue analysis. It revealed that EVOO lignans had promising T-cell immune anti-tumor activity in vitro and in vivo, particularly in a mice triple-negative breast cancer (TNBC) model; the lung metastasis was remarkably reduced about 59%, and improved 38% overall survival. Moreover, it synergized with anti-PD-1, boosting 53% efficacy. Furthermore, bioactivity-guided isolation revealed the compound (+)-matairesinol was identified as the potential T-cell immunomodulator, proteomic and phosphoproteomic analyses combined with blocking rescue experiments revealed that it promoted T-cell immune major through enhancing JAK3-STAT1 signal to upregulate granzyme B (GZMB), interferon gamma (IFN-γ) to kill multiple tumor cells. These findings could support EVOO to serve as dietary-based cancer prevention or combination immunotherapy and first revealed the T-cell immune anti-tumor mechanism and its bioactive compound involved in EVOO cancer prevention. - Source: PubMed
Publication date: 2026/04/27
Dai ZhiWang Xin-HuiXia MiaoLiu Fu-RaoYang Meng-JiaoLuo Xiao-Dong - Pulmonary fibrosis (PF) is a life-threatening interstitial lung disease characterized by scarring and inflammation in lung tissues. Aberrant activation of the JAK/STAT and NF-κB signaling pathways is critical in initiating and sustaining the inflammatory processes that drive fibrotic progression. In this study, we identify a novel small-molecule compound, T4015, a 4-indolyl-2-phenylaminopyrimidine derivative, as a dual-pathway inhibitor targeting both JAK/STAT and NF-κB signaling. Dual-luciferase reporter assays demonstrate the potent inhibitory activity of T4015 against these pathways. T4015 effectively suppresses the phosphorylation of STAT3, JAK1, and TYK2 induced by IL-6 and IFN-β, while suppressing LPS-induced NF-κB activation in macrophages. Transcriptome sequencing and pathway enrichment analyses further confirm that T4015 downregulates multiple inflammation-related signaling cascades, including the JAK/STAT, NF-κB, TNF, IL-17, and Toll-like receptor pathways. In a mouse model of bleomycin-induced PF, T4015 treatment significantly improves survival, attenuates collagen deposition, and reduces the expression of pro-inflammatory and profibrotic markers such as IL-6, CCL2, and COL1. Molecular docking and target prediction analyses suggest that T4015 exhibits strong binding affinity for multiple kinases within the JAK/STAT and NF-κB networks, including JAK1, TYK2, JAK2, JAK3, RIPK1, IRAK1/4, TAB1, and ZAP70. Collectively, these results highlight T4015 as a promising therapeutic candidate for PF through its simultaneous inhibition of the JAK/STAT and NF-κB signaling pathways. - Source: PubMed
Publication date: 2026/04/25
Zhang MinghuiXu HangLiu ShanXu XiaohanYin JiayiZhang XinxinZhang XiaonanYang XiaopingLiu XiaochunYin BinZhou MingmingWang LeweiZhang MengLiu HuiyingJiang WenqingSong QiaolingYang Jinbo