Ask about this productRelated genes to: Uhmk1 Blocking Peptide
- Gene:
- UHMK1 NIH gene
- Name:
- U2AF homology motif kinase 1
- Previous symbol:
- -
- Synonyms:
- KIS, Kist
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-12-09
- Date modifiied:
- 2016-10-05
Related products to: Uhmk1 Blocking Peptide
Related articles to: Uhmk1 Blocking Peptide
- Oral squamous cell carcinoma (OSCC) is a common malignant tumor in the head and neck region and clinically characterized by relatively high invasiveness and a propensity for metastasis. Patients generally exhibit nonsatisfactory prognosis. Beyond the classical endothelium-dependent angiogenesis pathway, vasculogenic mimicry (VM), a nonclassical blood supply mechanism whereby tumor cells themselves form microcirculatory conduits, plays a significant role in tumor progression. However, the regulatory mechanism of VM formation remains to be fully understood. U2AF homologous motif kinase 1 (UHMK1) is a regulatory protein possessing serine/threonine kinase activity and RNA-binding capability and was found to be overexpressed in OSCC tissues in our previous research. The present study aimed to explore the association between UHMK1 expression in OSCC and VM formation and elucidate the potential molecular mechanisms by which UHMK1 regulates VM development. Immunohistochemistry (IHC) results demonstrated that UHMK1 upregulation in OSCC was significantly correlated with VM structure, and both were associated with poor clinical outcomes and shortened patient survival time. In vitro experiments revealed that UHMK1 knockdown markedly suppressed VM formation in OSCC cells. Bioinformatics prediction and co-immunoprecipitation (co-IP) assays confirmed the interaction between UHMK1 and stathmin1 (STMN1). Further investigations indicated that UHMK1 stabilized STMN1 protein expression by inhibiting its ubiquitin-proteasome degradation pathway, and these two might jointly activate the PI3K/AKT/mTOR signaling pathway to regulate VM formation. The current study revealed the key role of UHMK1-STMN1 in coregulating VM formation in OSCC, providing new insights into the tumor microenvironment and identifying potential targets for anti-angiogenic therapy. - Source: PubMed
Publication date: 2026/04/09
Guo YanFeng YuanyongNi XiangningZhang XuanFang XiaoLi TongtongWang Ning - Circular RNAs (circRNAs) have emerged as critical regulators of colorectal cancer (CRC) progression; however, the biological function of circEIF2S2 remains largely unexplored. In this study, we investigated the expression, functional roles, and regulatory mechanisms of circEIF2S2 in CRC. Bioinformatic analyses and quantitative RT-PCR revealed that circEIF2S2 is significantly upregulated in CRC tissues and cell lines and is associated with unfavorable clinical outcomes. Functional assays demonstrated that circEIF2S2 silencing markedly suppressed CRC cell proliferation, migration, invasion, and immune checkpoint expression, while enhancing CD8 T cell-mediated immune responses in co-culture systems. Mechanistically, circEIF2S2 predominantly localized in the cytoplasm and functioned as a competing endogenous RNA by sponging miR-646, thereby relieving miR-646-mediated repression of UHMK1. In addition, the RNA-binding protein EIF4A3 promoted circEIF2S2 biogenesis through direct interaction with EIF2S2 pre-mRNA. Rescue experiments confirmed that the oncogenic and immunosuppressive effects of circEIF2S2 were partially reversed by miR-646 inhibition or UHMK1 suppression. In vivo, circEIF2S2 depletion significantly inhibited tumor growth and liver metastasis in xenograft models. Collectively, these findings identify the EIF4A3-circEIF2S2-miR-646-UHMK1 axis as an important regulatory pathway involved in CRC progression and tumor-associated immunosuppression. - Source: PubMed
Publication date: 2026/01/14
Fu XueZhang ZiDongNing DengLiu QiuMengZhao JunFangCheng QiChen XiaoPingJiang Li - U2AF homology motif kinase 1 (UHMK1) has been associated with RNA processing and protein phosphorylation, thereby influencing tumor progression. The study aimed to explore its regulatory mechanisms and biological functions in human prostate cancer (PCa). - Source: PubMed
Publication date: 2025/08/28
Zhang ChiHuang XiHu ChengTang BowenWu JianjieSun ZhuolunZhu WeianZhou XiangfuXiao HengjunWang Hua - Rheumatoid arthritis (RA) is an immune system disorder disease accompanied with severe joint damage. However, the molecular mechanism of RA with insensitive to medicine remains insufficient. Thus, this study aims to identify the biomarkers of RA patients with inadequate responses (IR) toward disease-modifying antirheumatic drug (DMARD) and antitumor necrosis factor (TNF) therapies, using multidimensional analyses. - Source: PubMed
Publication date: 2025/04/22
Li LeyuanGuo HuiZhang WeijinXiang XiChi JunZhang MengmengChen JialiWang ZhiminDai Liping - MicroRNAs are key post-transcriptional regulators of gene expression and their dysregulation is often linked to cancer. Epstein-Barr virus encodes 22 BamHI A Rightward Transcript (BART) miRNAs, which are expressed in nearly all EBV-associated cancers and implicated in viral pathogenesis. To investigate biological targets for BART miRNAs in B cell lymphomas, we performed a meta-analysis of publicly available Ago-CLIP datasets from EBV-positive Burkitt lymphomas (BLs), primary effusion lymphomas (PELs), AIDS-associated diffuse large B cell lymphomas (DLBCLs), and lymphoblastoid cell lines (LCLs). Our analysis focused on comparing targets of EBV BART miRNAs across the different types of transformed B cells. Using reporter assays, we then experimentally validated over 50 functional interactions between BART miRNAs and cellular protein-coding transcripts involved in activities such as B cell differentiation (, , and ), cell cycle regulation (, and T), apoptosis (), signaling and intracellular trafficking (, and ), and tumor suppression (). Moreover, ectopic BART miRNA expression in several EBV-negative BL cells induced transcriptional changes that may influence molecular signatures of EBV-associated BLs. Collectively, our findings reveal novel, functional interactions for BART miRNAs in lymphomas and provide insights into their roles in these B cell cancers. - Source: PubMed
Publication date: 2024/10/19
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