TESK2

Last update 08 May 2025

Basic Info

Synonyms

Dual specificity testis-specific protein kinase 2, TESK2, Testicular protein kinase 2

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Introduction

Dual specificity protein kinase activity catalyzing autophosphorylation and phosphorylation of exogenous substrates on both serine/threonine and tyrosine residues. Phosphorylates cofilin at 'Ser-3'. May play an important role in spermatogenesis.

100 Clinical Results associated with TESK2

100 Translational Medicine associated with TESK2

0 Patents (Medical) associated with TESK2

Literatures (Medical) associated with TESK2

01 Dec 2022·Clinical Epigenetics

Epimutations in both the TESK2 and MMACHC promoters in the Epi-cblC inherited disorder of intracellular metabolism of vitamin B12

Article

Author: Hergalant, Sébastien ; Guerrini, Renzo ; Guéant, Jean-Louis ; Morange, Pierre-Emmanuel ; Rouyer, Pierre ; Cavicchi, Catia ; Rosenblatt, David S ; Froese, D Sean ; Siblini, Youssef ; Chéry, Céline ; Pupavac, Mihaela ; Morrone, Amelia ; Ficicioglu, Can ; Trégouët, David ; Watkins, David ; Majewski, Jacek ; Oussalah, Abderrahim ; Benoist, Jean-François ; Feillet, François ; Pastinen, Tomi ; Baumgartner, Matthias R ; Chung, Wendy K

AbstractBackgroundepi-cblCis a recently discovered inherited disorder of intracellular vitamin B12metabolism associating hematological, neurological, and cardiometabolic outcomes. It is produced by an epimutation at the promoter common toCCDC163PandMMACHC, which results from an aberrant antisense transcription due to splicing mutations in the antisensePRDX1gene neighboringMMACHC. We studied whether the aberrant transcription produced a second epimutation by encompassing the CpG island of theTESK2gene neighboringCCDC163P.MethodsWe unraveled the methylome architecture of theCCDC163P–MMACHCCpG island (CpG:33) and theTESK2CpG island (CpG:51) of 17 epi-cblCcases. We performed an integrative analysis of the DNA methylome profiling, transcriptome reconstruction of RNA-sequencing (RNA-seq), chromatin immunoprecipitation sequencing (ChIP-Seq) of histone H3, and transcription expression ofMMACHCandTESK2.ResultsThePRDX1splice mutations and activation of numerous cryptic splice sites produced antisense readthrough transcripts encompassing the bidirectionalMMACHC/CCDC163Ppromoter and theTESK2promoter, resulting in the silencing of both theMMACHCandTESK2genes through the deposition of SETD2-dependent H3K36me3 marks and the generation of epimutations in the CpG islands of the two promoters.ConclusionsThe antisense readthrough transcription of the mutatedPRDX1produces an epigenetic silencing ofMMACHCandTESK2. We propose using the term 'epi-digenism' to define this epigenetic disorder that affects two genes. Epi-cblCis an entity that differs fromcblC.Indeed, thePRDX1 and TESK2altered expressions are observed in epi-cblCbut not incblC, suggesting further evaluating the potential consequences on cancer risk and spermatogenesis.

01 Sep 2018·Cancer ResearchQ1 · MEDICINE

Therapeutic Targeting of the Premetastatic Stage in Human Lung-to-Brain Metastasis

Q1 · MEDICINE

Article

Author: Tokar, Tomas ; Singh, Sheila K. ; Vora, Parvez ; McFarlane, Nicole ; Murty, Naresh K. ; Bakhshinyan, David ; Jurisica, Igor ; Subapanditha, Minomi K. ; Venugopal, Chitra ; Qazi, Maleeha ; Singh, Mohini

AbstractBrain metastases (BM) result from the spread of primary tumors to the brain and are a leading cause of cancer mortality in adults. Secondary tissue colonization remains the main bottleneck in metastatic development, yet this “premetastatic” stage of the metastatic cascade, when primary tumor cells cross the blood–brain barrier and seed the brain before initiating a secondary tumor, remains poorly characterized. Current studies rely on specimens from fully developed macrometastases to identify therapeutic options in cancer treatment, overlooking the potentially more treatable “premetastatic” phase when colonizing cancer cells could be targeted before they initiate the secondary brain tumor. Here we use our established brain metastasis initiating cell (BMIC) models and gene expression analyses to characterize premetastasis in human lung-to-BM. Premetastatic BMIC engaged invasive and epithelial developmental mechanisms while simultaneously impeding proliferation and apoptosis. We identified the dopamine agonist apomorphine to be a potential premetastasis-targeting drug. In vivo treatment with apomorphine prevented BM formation, potentially by targeting premetastasis-associated genes KIF16B, SEPW1, and TESK2. Low expression of these genes was associated with poor survival of patients with lung adenocarcinoma. These results illuminate the cellular and molecular dynamics of premetastasis, which is subclinical and currently impossible to identify or interrogate in human patients with BM. These data present several novel therapeutic targets and associated pathways to prevent BM initiation.Significance: These findings unveil molecular features of the premetastatic stage of lung-to-brain metastases and offer a potential therapeutic strategy to prevent brain metastases. Cancer Res; 78(17); 5124–34. ©2018 AACR.

15 Jun 2017·Human Molecular GeneticsQ2 · BIOLOGY

Discovery of novel heart rate-associated loci using the Exome Chip

Q2 · BIOLOGY

Article

Author: Morris, Andrew D ; Dedoussis, George ; Vaartjes, Ilonca ; Smith, Albert V ; Rotter, Jerome I ; Verweij, Niek ; Qi, Lihong ; Cabrera, Claudia P ; Warren, Helen R ; Lin, Honghuang ; van den Berg, Marten E ; Gudnason, Vilmundur ; Mook-Kanamori, Dennis O ; Silva, Claudia T ; Psaty, Bruce M ; Jamshidi, Yalda ; Hagemeijer, Yanick ; Ellinor, Patrick T ; Eijgelsheim, Mark ; van der Meer, Peter ; Launer, Lenore J ; Entwistle, Aiman ; Porteous, David J ; Trompet, Stella ; Peters, Annette ; Uitterlinden, André ; Spector, Timothy D ; Stanton, Alice V ; Sotoodehnia, Nona ; Doney, Alex S F ; Stirrups, Kathleen E ; de Haan, Hugoline G ; Huang, Paul L ; Yao, Jie ; Marten, Jonathan ; Taylor, Kent D ; Harris, Tamara B ; de Mutsert, Renée ; Kähönen, Mika ; Arking, Dan E ; Pedersen, Oluf ; Liu, Simin ; Weiss, Stefan ; Lubitz, Steven A ; Kolcic, Ivana ; Hayward, Caroline ; Shah, Nabi ; Sattar, Naveed ; Raitakari, Olli T ; Alonso, Alvaro ; Müller-Nurasyid, Martina ; Munroe, Patricia B ; Tinker, Andrew ; Deloukas, Panos ; van der Harst, Pim ; Hoes, Arno W ; Palmer, Colin N A ; Soliman, Elsayed Z ; Li, Man ; Sinner, Moritz F ; Tobin, Martin D ; Lyytikäinen, Leo-Pekka ; Mangino, Massimo ; Mifsud, Borbala ; Waldenberger, Melanie ; Mulas, Antonella ; Prins, Bram P ; Lehtimäki, Terho ; Dörr, Marcus ; Isaacs, Aaron ; Murray, Alison D ; Hansen, Torben ; Orrú, Marco ; Guo, Xiuqing ; Samani, Nilesh J ; Haessler, Jeffrey ; Linneberg, Allan ; Xie, Zhijun ; Radmanesh, Farid ; Polasek, Ozren ; Bihlmeyer, Nathan A ; Dominiczak, Anna F ; Kors, Jan A ; de Boer, Rudolf ; Rivadeneira, Fernando ; Bis, Joshua C ; Fu, Yi-Ping ; Felix, Stephan B ; van Setten, Jessica ; Kääb, Stefan ; Poulter, Neil ; Pistis, Giorgio ; van Duijn, Cornelia M ; Kooperberg, Charles ; Brody, Jennifer A ; Grarup, Niels ; Jukema, J Wouter ; O'Donnell, Chris J ; Zoledziewska, Magdalena ; Hwang, Shih-Jen ; Eppinga, Ruben N ; Caulfield, Mark J ; Stricker, Bruno H ; Hall, Leanne M ; Mei, Hao ; Nelson, Christopher P ; Heckbert, Susan R ; Wilson, James ; Padmanabhan, Sandosh ; Sanna, Serena ; Rosand, Jonathan ; Li-Gao, Ruifang ; Zeggini, Eleftheria ; Asselbergs, Folkert W ; Lin, Henry J ; Völker, Uwe ; Macfarlane, Peter W ; Rudan, Igor ; Kanters, Jørgen K ; Sever, Peter ; Roselli, Carolina

Resting heart rate is a heritable trait, and an increase in heart rate is associated with increased mortality risk. Genome-wide association study analyses have found loci associated with resting heart rate, at the time of our study these loci explained 0.9% of the variation. This study aims to discover new genetic loci associated with heart rate from Exome Chip meta-analyses.Heart rate was measured from either elecrtrocardiograms or pulse recordings. We meta-analysed heart rate association results from 104 452 European-ancestry individuals from 30 cohorts, genotyped using the Exome Chip. Twenty-four variants were selected for follow-up in an independent dataset (UK Biobank, N = 134 251). Conditional and gene-based testing was undertaken, and variants were investigated with bioinformatics methods.We discovered five novel heart rate loci, and one new independent low-frequency non-synonymous variant in an established heart rate locus (KIAA1755). Lead variants in four of the novel loci are non-synonymous variants in the genes C10orf71, DALDR3, TESK2 and SEC31B. The variant at SEC31B is significantly associated with SEC31B expression in heart and tibial nerve tissue. Further candidate genes were detected from long-range regulatory chromatin interactions in heart tissue (SCD, SLF2 and MAPK8). We observed significant enrichment in DNase I hypersensitive sites in fetal heart and lung. Moreover, enrichment was seen for the first time in human neuronal progenitor cells (derived from embryonic stem cells) and fetal muscle samples by including our novel variants.Our findings advance the knowledge of the genetic architecture of heart rate, and indicate new candidate genes for follow-up functional studies.

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TESK2

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