STK10

Last update 08 May 2025

Basic Info

Synonyms

LOK, Lymphocyte-oriented kinase, PRO2729

+ [3]

Introduction

Serine/threonine-protein kinase involved in regulation of lymphocyte migration. Phosphorylates MSN, and possibly PLK1. Involved in regulation of lymphocyte migration by mediating phosphorylation of ERM proteins such as MSN. Acts as a negative regulator of MAP3K1/MEKK1. May also act as a cell cycle regulator by acting as a polo kinase kinase: mediates phosphorylation of PLK1 in vitro; however such data require additional evidences in vivo.

100 Clinical Results associated with STK10

100 Translational Medicine associated with STK10

0 Patents (Medical) associated with STK10

Literatures (Medical) associated with STK10

02 Apr 2025·Journal of Psychiatry and Neuroscience

Genome-wide DNA methylation profiling of blood samples from patients with major depressive disorder: correlation with symptom heterogeneity

Article

Author: Kameyama, Shinichi ; Kanai, Yae ; Fujimoto, Mao ; Nagao, Yukiko ; Arai, Eri ; Hattori, Kotaro ; Kunugi, Hiroshi ; Hidese, Shinsuke ; Tian, Ying

BACKGROUNDAlterations in DNA, such as DNA methylation, may be key molecular events involved in the development of major depressive disorder (MDD). We sought to clarify correlations between DNA methylation profiles and symptom heterogeneity among patients with MDD.METHODSWe conducted a genome-wide DNA methylation analysis of blood samples from patients with MDD and controls, using the Infinium MethylationEPIC BeadChip.RESULTSWe analyzed 283 blood samples, including 141 from an initial cohort (69 patients with MDD, 72 controls) and 142 from a second validation cohort (67 patients with MDD, 75 controls). After adjustment for age, sex, and blood cell heterogeneity, DNA methylation status at 2699 CpG sites tended to differ between patients with MDD and controls in both the initial and second cohorts. Hierarchical clustering of patients based on DNA methylation status at these 2699 CpG sites revealed a significant correlation with scores for GRID-Hamilton Depression Rating Scale (GRID-HAMD) items (depressed mood, guilt, early insomnia, middle insomnia, work and activities, psychic anxiety, loss of appetite, general somatic symptoms, and total score), suggesting the feasibility of severity diagnostics based on blood DNA methylation testing. Pathway over-representation analysis revealed that genes whose DNA methylation status was correlated with epigenetic clustering were accumulated in molecular pathways involved in various cellular functions, especially nerve development. For PLEKHD1, STK10, and FOXK1, DNA methylation levels were inversely correlated with expression levels in the Clinical Proteomic Tumor Analysis Consortium database. DNA hypomethylation of PLEKHD1, STK10, and FOXK1 was correlated with higher GRID-HAMD scores in both cohorts.LIMITATIONSAlthough we performed marker exploration using 2 cohorts including 283 participants, the heterogeneity of the molecular mechanisms operating in MDD might necessitate a larger cohort for establishment of criteria with sufficient diagnostic impact.CONCLUSIONThese findings indicate that the DNA methylation status of specific genes may correlate with the severity of MDD symptoms, and that genome-wide DNA methylation analysis of blood samples would be useful for clarifying the DNA methylation profiles related to symptom heterogeneity.

06 Sep 2024·Science Advances

Excitable Rho dynamics control cell shape and motility by sequentially activating ERM proteins and actomyosin contractility

Article

Author: Umar, Mustakim ; Migueles-Ramírez, Rodrigo A. ; El Baba, Nada ; Mavalwala, Kian ; Marshall-Burghardt, Seph ; Hayer, Arnold ; Lin, Qiyao ; Saada, Rayan

Migration of endothelial and many other cells requires spatiotemporal regulation of protrusive and contractile cytoskeletal rearrangements that drive local cell shape changes. Unexpectedly, the small GTPase Rho, a crucial regulator of cell movement, has been reported to be active in both local cell protrusions and retractions, raising the question of how Rho activity can coordinate cell migration. Here, we show that Rho activity is absent in local protrusions and active during retractions. During retractions, Rho rapidly activated ezrin-radixin-moesin proteins (ERMs) to increase actin-membrane attachment, and, with a delay, nonmuscle myosin 2 (NM2). Rho activity was excitable, with NM2 acting as a slow negative feedback regulator. Strikingly, inhibition of SLK/LOK kinases, through which Rho activates ERMs, caused elongated cell morphologies, impaired Rho-induced cell contractions, and reverted Rho-induced blebbing. Together, our study demonstrates that Rho activity drives retractions by sequentially enhancing ERM-mediated actin-membrane attachment for force transmission and NM2-dependent contractility.

01 Aug 2024·Annals of Hematology

STK10 mutations block erythropoiesis in acquired pure red cell aplasia via impairing ribosome biogenesis

Article

Author: Yang, Jichun ; Long, Zhangbiao ; Zhou, Xun ; Qiao, Xinrui ; Han, Bing ; Chen, Miao ; Shi, Xiaofeng ; Liu, Xinyao ; Li, Hongmin ; Fang, Dongdong ; Du, Yali

Acquired pure red cell aplasia (PRCA) is anemia associated with the absence of erythroblasts and is characterized by persistent and easy recurrence. However, the underlying mechanisms of acquired PRCA remain obscure, and the role of gene mutations in the pathogenesis of acquired PRCA is not fully characterized. In the present study, we detected thirty newly diagnosed patients with acquired PRCA using whole exome sequencing, and a potential role for STK10 in acquired PRCA was uncovered. The mRNA levels of STK10 in three patients with STK10 mutations were decreased. These three patients had a poor response to immunosuppressive therapy and two died in the follow-up period. Here we report that knockdown of STK10 inhibits erythroid differentiation and promotes apoptosis of K562 cells. We show that knockdown of STK10 resulted in inhibition of ribosome biogenesis and reduced ribosome levels in K562 cells. We also show that the p53 signaling pathway is activated by knockdown of STK10. Our results imply that ribosome biogenesis downregulation together with pathological p53 activation prevents normal erythropoiesis. Our study uncovers a new pathophysiological mechanism leading to acquired PRCA driven by STK10 mutations.

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STK10

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