TG-101348 Mechanisms: JAK2 inhibitor
- Known as:
- TG-101348 Mechanisms: JAK2 suppressor
- Catalog number:
- A-1140
- Product Quantity:
- 5mg
- Category:
- -
- Supplier:
- Activ
- Gene target:
- TG-101348 Mechanisms: JAK2 inhibitor
Related genes to: TG-101348 Mechanisms: JAK2 inhibitor
- 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: TG-101348 Mechanisms: JAK2 inhibitor
Related articles to: TG-101348 Mechanisms: JAK2 inhibitor
- In colorectal cancer (CRC), metastasis drives fatalities, necessitating the discovery of therapeutic targets modulating its progression. Though the secreted protein-coding gene leucine-rich repeat neuronal 4 (LRRN4) was shown to be highly overexpressed in CRC and linked to decreased survival in the analysis of TCGA-CRC datasets, little is known about its function as well as mechanism in CRC metastasis. Thus, our work aimed to investigate LRRN4 functions and its role in CRC metastasis. We first confirmed that CRC metastasis was related to raised LRRN4 expression in CRC tissues. LRRN4 depletion using siRNA/shRNA inhibited CRC metastasis in vitro and in vivo, decreasing vimentin and increasing E-cadherin levels, whereas its overexpression yielded opposite effects. Mechanistically, LRRN4 promoted CRC metastasis by upregulating IL23A expression and triggering JAK2-STAT3 signaling, as evidenced by LRRN4 depletion-reduced IL23A expression and downstream JAK2-STAT3 activity; the STAT3 inhibitor and recombinant human IL23 protein rescued the promotion and inhibition of cell migration induced by LRRN4 overexpression and knockdown, respectively. Kaplan-Meier analysis and the K-independent samples nonparametric test revealed that the upregulated marker proportion was positively related to the likelihood of metastases, and people having raised IL23A and LRRN4 levels had the lowest survival. Finally, elevated LRRN4 expression in CRC tissues was correlated with promoter hypomethylation. Thus, LRRN4 is upregulated by promoter DNA hypomethylation, and the LRRN4-IL23A-JAK2-STAT3 axis is a critical driver of CRC metastasis, representing a promising therapeutic target and prognostic biomarker. - Source: PubMed
Publication date: 2026/08/20
Lin JiatianMin ShashaLi ZesongWang YujieLi HonghuiZhang XigangXie Xina - Cytopenia represents a distinct clinical phenotype in primary myelofibrosis (PMF), often associated with advanced disease and poor prognosis. We propose that while a common driver mutation initiates the disease, the clinical phenotype of PMF is shaped by inter-individual variability in downstream inflammatory responses, contributing to the observed heterogeneity in disease presentation. - Source: PubMed
Publication date: 2026/08/18
Lee Sze-HweiWang Yu-HungChang Yu-SungWei Chao-HungYuan Chang-TsuHou Hsin-AnChou Wen-ChienTien Hwei-FangLin Chien-Chin - Myeloid neoplasms harboring both an isolated deletion of chromosome 5q (del(5q)) and myeloproliferative neoplasm (MPN) driver mutations () constitute a rare and diagnostically challenging subset, often described with features overlapping those of myelodysplastic syndromes (MDS) and MPN. - Source: PubMed
Publication date: 2026/08/17
Abdulgayoom MohammedAl-Mashdali Abdulrahman FAlshurafa AwniAfana Mohammad SBabiker Anas MBakheet MohammadMohamed Shehab FYassin Mohamed A - The loss of IFNγ signaling in cancer cells causes primary and acquired resistance to immunotherapy. Using a patient-derived JAK2-deficient melanoma cell line, we have developed a co-culture system to model acquired resistance to immunotherapy. Genome-wide genetic screens uncover that protein neddylation can be targeted to restore sensitivity to PD1 blockade in co-cultures, and in MHC-I and/or JAK/STAT-deficient murine tumors. Analysis of the Jak2-deficient murine tumors with scRNA-seq reveals a heightened cancer-intrinsic inflammatory signature when neddylation is absent, which causes an influx of stimulatory antigen presenting cells. In patients with melanoma, tumors with low cancer-intrinsic neddylation exhibit elevated IFN signatures and are associated with dendritic cell infiltration. Mechanistically, neddylation deletion stabilizes chromatin-bound cGAS in JAK2-deficient cancer cells, which is responsible for the superior response to PD1 blockade, and the recruitment of pro-inflammatory innate immune cells. Altogether, we demonstrate the broad therapeutic potential of protein neddylation in overcoming resistance to immunotherapy. - Source: PubMed
Publication date: 2026/08/06
Mao YumengBedos Marta RubiesLu YonglinVoutsinou EiriniPapakyriacou IrineosAlford LiamParracho RebecaIyer VaishnaviRibas Antoni - A middle-aged adult presented with non-severe alcoholic hepatitis after 3 years of daily whisky intake (80-100 mL/day). He was noted to have persistent erythrocytosis (haemoglobin 186 g/L; haematocrit 53.8%) without leucocytosis or thrombocytosis and with normal serum erythropoietin. Secondary causes were evaluated, including hypoxia, cardiac and renal disease, and myeloproliferative neoplasms; Janus Kinase 2 Valine 617 Phenylalanine (JAK2 V617F) and JAK 2 exon 12 testing were negative. Despite intravenous hydration and reported complete alcohol abstinence, erythrocytosis persisted for several weeks after hepatic biochemistry improved. A bone marrow biopsy was planned but deferred when haemoglobin and haematocrit normalised spontaneously by 10 weeks. Overall, the presentation was most consistent with presumed alcohol-associated stress (relative) erythrocytosis, which may show delayed resolution after cessation, and careful longitudinal follow-up may avoid premature invasive investigations once polycythaemia vera and clinically important secondary causes have been reasonably excluded. - Source: PubMed
Publication date: 2026/08/19
Saquib Alam MohammadZafar Khwaja Saifullah