Ask about this productRelated genes to: STAT5B Blocking Peptide
- Gene:
- STAT5B NIH gene
- Name:
- signal transducer and activator of transcription 5B
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-01-28
- Date modifiied:
- 2019-04-23
Related products to: STAT5B Blocking Peptide
Related articles to: STAT5B Blocking Peptide
- Glioblastoma (GBM) is driven, in part, by glioma stem cells (GSCs), which sustain therapeutic resistance and recurrence. OLIG2 is a key regulator of GSC programs but the signaling pathways that cooperate with Oligodendrocyte transcription factor 2 (OLIG2) to maintain GSC states remain incompletely defined. Although Signal transducer and activator of transcription (STAT) signaling has been implicated in GSC biology, work to date has focused primarily on STAT3, and the contribution of STAT5 remains poorly defined. Here, we investigated whether STAT5B functionally cooperates with OLIG2 in sustaining GSC phenotypes. - Source: PubMed
Publication date: 2026/05/12
Miller AunayMcNamara JamesBlomquist Mylan RNascari DavidFlick MatthewSaladin SidneyTuncali SerdarSereduk ChristopherOrndorf KeelyEnsign Shannon P FortinLoftus Joseph CTran Nhan LMehta Shwetal - Chemotherapy is the primary mode of treatment for patients with advanced bladder cancer. However, because of their non-specificity, chemotherapy drugs induce many notable side effects in patients. Recent studies have shown that the expression of certain long non-coding RNAs (lncRNAs) is closely related to the sensitivity of tumors to chemotherapeutic drugs. Thus, lncRNAs can be exploited as markers of tumor chemotherapeutic sensitivity to improve the efficacy of chemotherapy. Here, we investigated the role of the lnc00892 in the response of bladder cancer cells to cisplatin. - Source: PubMed
Publication date: 2026/05/27
Chang YixinSun NingLiu YijieJin ZihuiZhang PeipeiWang SijiaChen JieLiu JiantingLin ZhenniLu YongyongHuang HaishanHuang ChuanshuJin Honglei - Mutations in cytokine receptor and JAK/STAT; Cy-JAK/STAT) signaling genes drive myeloproliferative neoplasms (MPNs) but remain incompletely characterized in acute myeloid leukemia (AML). The authors evaluated the prevalence, clinical presentation, and prognostic significance of Cy-JAK/STAT pathway mutations in patients with AML and compared outcomes across disease ontogeny. - Source: PubMed
Albliwi MoathNurse Daniel PZabor Emily CHanna JohnEl-Asmar JessicaBawwab AmeedAbuamsha HasanAbu-Farsakh YomnaBatah HeyaRauf AsadNakitandwe JoyBosler David SParthasarathy Prerana BangaloreAlban TylerJain Akriti GMolina John CBalderman SophiaSingh AbhayGerds Aaron TMukherjee SudiptoAdvani Anjali SCarraway Hetty EMustafa Ali Moaath K - Interferon regulatory factors (IRFs) are innate immune transcription factors responsible for inducing the expression of type I interferons (IFN-I), which combat pathogen invasions via initiating the downstream Janus kinase signal transducer and activator of transcription (JAK-STAT) pathway. Among them, IRF7 plays a central role by forming heterodimers with IRF3 to initiate IFN-I production and is therefore frequently targeted by viruses to evade immune detection. Contrary to this common paradigm, we show that IRF7 is activated and upregulated by the retrovirus human T-cell leukemia virus type 1 (HTLV-1), via its oncoprotein HBZ. Moreover, IRF7 is highly expressed in HTLV-1 induced CD4 T-cell malignancy named adult T-cell leukemia/lymphoma (ATLL), and promotes the proliferation of infected cells both in vitro and in vivo. Intriguingly, HBZ is able to interfere with the interaction of IRF7 and IRF3, suppressing IFN-I pathway activation. On the other hand, IRF7 was found to upregulate and activate STAT5B, a transcription factor of the JAK-STAT pathway frequently mutated in hematological malignancies. Together, these findings reveal a mechanism by which HTLV-1 hijacks a critical innate immune effector to sustain persistent infection and drive oncogenesis without activating antiviral IFN-I pathway. - Source: PubMed
Publication date: 2026/05/11
Yuan XiaoyiYue YunyunChen LiangLiu DongmeiLiang YiLu ChengchengYang SikaiHe ZengFan ChunxinShang JingMatsuoka MasaoMa Guangyong - In flatfish aquaculture, labour-intensive tank cleaning represents a major operational challenge, limiting sustainability due to its high labour requirements and associated costs. We tested a new semi-closed recirculating aquaculture system (RAS) protocol for (tongue sole), replacing manual cleaning with post-feeding water exchange (80% drained) and probiotic application. Compared with control groups, the probiotic-water exchange protocol significantly improved growth (+0.18%/day) and survival (+7.9%), while shifting the gut microbiota from a -dominated configuration to a -dominated one. Metagenomics revealed that became the predominant taxon (86%) in the probiotic group, accompanied by the enrichment of quorum sensing pathways, CAZymes (CEs, AAs), and nutrient metabolism functions. Histological examination showed improvements in the intestinal muscular layer and villi structure. Multi-tissue transcriptomics identified systemic changes in immune and metabolic pathways, including activation of intestinal immune networks (IgA production, NF-κB signaling) and antimicrobial peptide genes. Liver, gill, and skin transcriptomes revealed enhanced DNA repair, cytokine signaling, and barrier pathways. JAK-STAT pathway was also activated, linking microbial metabolite sensing to growth promotion (). The probiotic-integrated protocol modifies the gut microbiome by shifting microbial composition through changes in competitive interactions and microbial signaling pathways. It also improves the intestinal wall, overall immunity, and nutrient absorption. These findings provide insights into the microbiome-host interaction under probiotic treatment and suggest that this strategy may offer potential benefits under farm conditions, but further studies are needed to validate its safety and ecological implications. - Source: PubMed
Publication date: 2026/04/23
Hu YuanriYan XuGao FengtaoXu DanYang YingmingCheng JiayuChen SonglinCui Zhongkai