ULK4

Last update 08 May 2025

Basic Info

Synonyms

FAM7C1, FLJ20574, REC01035

+ [5]

Introduction

May be involved in the remodeling of cytoskeletal components, such as alpha-tubulin, and in this way regulates neurite branching and elongation, as well as cell motility.

100 Clinical Results associated with ULK4

100 Translational Medicine associated with ULK4

0 Patents (Medical) associated with ULK4

Literatures (Medical) associated with ULK4

12 Feb 2025·Endocrine, Metabolic & Immune Disorders - Drug Targets

Prediction of the Prognosis and Treatment Responses Based on the Characteristics of Disulfidptosis-Related Genes in Patients with Cervical Squamous Cell Carcinoma and Endocervical Adenocarcinoma

Article

Author: Xu, Youhua ; Jiang, Sha ; Kang, Min ; Mo, Hui ; Chen, Huihui

Background:Disulfidptosis is a new type of regulatory cell death (RCD), but the pathophysiological functions and mechanisms of DRGs in CESC remain to be examined.Aims:This study explored the mutation status of disulfidptosis-related genes (DRGs) in cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC).Objective:After analyzing the mutation profiles of DRGs in CESC, this study established a prognostic model for CESC and also explored the differences in immune infiltration (accumulation of immune system cells in tissues or organs), related enriched pathways, and drug sensitivity between high-risk and low-risk CESC groups.Methods:The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) were accessed to source related data. The mutation profiles of DRGs in CESC were analyzed using Mutect2 software, and disulfidptosis scores were calculated by ssGSEA. WGCNA was performed to identify modular genes, which were further filtered and used to formulate a risk model by applying the survival and glmnet packages. Low- and high-risk groups of CESC patients were classified using the survminer package. GSEA was performed to conduct pathway analysis, and immune infiltration was assessed using the MCPcounter package, ESTIMATE, and TIMER algorithms. Finally, immunotherapy response and drug sensitivity were analyzed using the TIDE method and the pRRophetic package, respectively.Results:Except for NDUFA11, ARL6IP5, EPM2AIP1, GBE1, RBM38, ULK4, and ZBTB47 were found to be the DRGs significantly mutated in CESC. The six genes were integrated to develop a RiskScore model with a relatively high Area Under the Curve (AUC) value. Significant differences between the two risk groups were determined, indicating that the model was highly reliable. Notably, the low-risk group was enriched in energy metabolism-correlated pathways, while the high-risk group was primarily enriched in immune-correlated pathways. The high-risk group showed higher immune cell activity, higher TIDE score, and more B cells than the low-risk group. Drug sensitivity study revealed that the high-risk group was more sensitive to chemotherapy drugs.Conclusion:This study provides novel insights into CESC prognosis, immunotherapy, and drug development, contributing to the clinical treatment for CESC.

01 Sep 2024·American Journal of Physiology-Lung Cellular and Molecular Physiology

Obesity impairs ciliary function and mucociliary clearance in the murine airway epithelium

Article

Author: Ohta, Isao ; Furuhashi, Kazuki ; Hozumi, Hironao ; Inui, Naoki ; Suda, Takafumi ; Setou, Mitsutoshi ; Enomoto, Noriyuki ; Suzuki, Tetsuro ; Takaku, Yasuharu ; Suzuki, Yuzo ; Yasui, Hideki ; Inoue, Yusuke ; Yazawa, Shusuke ; Ito, Masahiko ; Karayama, Masato ; Tanaka, Yuko ; Fujisawa, Tomoyuki

Our study shows that obesity impairs airway mucociliary clearance (MCC), an essential physical innate defense mechanism for viral infection. Mechanically, this is likely due to the obesity-induced downregulation of cilia-related genes and attenuation of extracellular ATP release. This study provides novel insights into the mechanisms driving the higher susceptibility and severity of viral respiratory infections in individuals with obesity.

01 Sep 2023·The FASEB Journal

The putative protein kinase Stk36 is essential for ciliogenesis and CSF flow by associating with Ulk4

Article

Author: Yang, Meimei ; Liu, Min ; Yang, Fan ; Gong, Xuanwei ; Liu, Jiaxin ; Zhang, Hongye ; Zhang, Jianhua ; Han, Yongfeng ; Shen, Sanbing ; Guan, Tianyuan ; Li, Li

AbstractMotile cilia lining on the ependymal cells are crucial for cerebrospinal fluid (CSF) flow and its dysfunction is often associated with hydrocephalus. Unc51‐like‐kinase 4 (Ulk4) was previously linked to CSF flow and motile ciliogenesis in mice, as the hypomorph mutant of Ulk4 (Ulk4tm1a/tm1a) developed hydrocephalic phenotype resulted from defective ciliogenesis and disturbed ciliary motility, while the underling mechanism is largely obscure. Here, we report that serine/threonine kinase 36 (STK36), a paralog of ULK4, directly interacts with ULK4 and this was demonstrated by yeast two‐hybrid (Y2H) in yeast and coimmunoprecipitation (co‐IP) assays in HEK293T cells, respectively. The interaction region was confined to their respective N‐terminal kinase domain. The hypomorph mutant of Stk36 (Stk36tmE4−/−) also developed progressive hydrocephalus postnatally and dysfunctional CSF flow, with multiple defects of motile cilia, including reduced ciliary number, disorganized ciliary orientation, defected axonemal structure and inconsistent base body (BB) orientation. Stk36tmE4−/− also disturbed the expression of Foxj1 transcription factor and a range of other ciliogenesis‐related genes. All these morphological changes, motile cilia defects and transcriptional dysregulation in the Stk36tmE4−/− are practically copied from that in Ulk4tm1a/tm1a mice. Taken together, we conclude that both Stk36 and Ulk4 are crucial for CSF flow, they cooperate by direct binding with their kinase domain to regulate the Foxj1 transcription factor pathways for ciliogenesis and cilia function, not limited to CSF flow. The underlying molecular mechanism probably conserved in evolution and could be extended to other metazoans.

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