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CDC-like kinase 2

CLK2, hClk2
This gene encodes a member of the CLK family of dual specificity protein kinases. CLK family members have been shown to interact with, and phosphorylate, serine- and arginine-rich (SR) proteins of the spliceosomal complex, which is a part of the regulatory mechanism that enables the SR proteins to control RNA splicing. Note that this gene is distinct from TELO2 gene (GeneID:9894), which shares CLK2 and hCLK2 symbol aliases in common with this gene, but encodes a protein that is involved in telomere length regulation. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Clk, p53, FAN, CAN, Hus1
Papers on CLK2
An epigenetic signal encoded protection mechanism is activated by graphene oxide to inhibit its induced reproductive toxicity in Caenorhabditis elegans.
Wang et al., Nanjing, China. In Biomaterials, Feb 2016
For the underlying molecular mechanism of reproductive toxicity of GO, we raised a signaling cascade of HUS-1/CLK-2-CEP-1-EGL-1-CED-4-CED-3 to explain the roles of core apoptosis signaling pathway and DNA damage checkpoints.
Benzobisthiazoles Represent a Novel Scaffold for Kinase Inhibitors of CLK Family Members.
Ketteler et al., London, United Kingdom. In Biochemistry, Feb 2016
Here, we have developed a screening workflow for the identification of potent CLK2 inhibitors and identified compounds with a novel chemical scaffold structure, the benzobisthiazoles, that has not been previously reported for kinase inhibitors.
CLK2 Is an Oncogenic Kinase and Splicing Regulator in Breast Cancer.
Polyak et al., Seoul, South Korea. In Cancer Res, May 2015
Here, we report that CLK2, a kinase that phosphorylates SR proteins involved in splicing, acts as an oncogene in breast cancer.
Alterations in Caenorhabditis elegans and Cronobacter sakazakii lipopolysaccharide during interaction.
Balamurugan et al., Kāraikkudi, India. In Arch Microbiol, Mar 2015
atf-7, scl-2, cpr-2) and aging-related genes (skn-1, clk-2, bra-2, age-1, bec-1, daf-16, daf-2).
Identifying three-dimensional structures of autophosphorylation complexes in crystals of protein kinases.
Dunbrack et al., Philadelphia, United States. In Sci Signal, 2014
These five complexes consist of tyrosine residues in the N-terminal juxtamembrane regions of colony-stimulating factor 1 receptor (CSF1R, Tyr(561)) and ephrin receptor A2 (EPHA2, Tyr(594)), tyrosine residues in the activation loops of the SRC kinase family member LCK (Tyr(394)) and insulin-like growth factor 1 receptor (IGF1R, Tyr(1166)), and a serine in a nuclear localization signal region of CDC-like kinase 2 (CLK2, Ser(142)).
Computational & experimental evaluation of the structure/activity relationship of β-carbolines as DYRK1A inhibitors.
Schmidt et al., Darmstadt, Germany. In Bioorg Med Chem Lett, 2014
Furthermore we identified a modified lead structure as a potent DYRK1A inhibitor (IC50=130 nM) with significant selectivity against MAO-A, DYRK2, DYRK3, DYRK4 & CLK2.
The roles of DNA damage-dependent signals and MAPK cascades in tributyltin-induced germline apoptosis in Caenorhabditis elegans.
Xie et al., Huainan, China. In Chemosphere, 2014
Checkpoint proteins HUS-1 and CLK-2 exerted proapoptotic effects, and the null mutation of cep-1, the homologue of tumor suppressor gene p53, significantly inhibited TBT-induced apoptosis.
Human CDC2-like kinase 1 (CLK1): a novel target for Alzheimer's disease.
Trivedi et al., Bhopāl, India. In Curr Drug Targets, 2014
The CLK family consists of four isoforms namely CLK1, CLK2, CLK3 and CLK4.
IR laser-induced protein crystal transformation.
Huber et al., Martinsried, Germany. In Acta Crystallogr D Biol Crystallogr, 2014
Heating proved superior to traditional controlled dehydration by humidity change for the test cases CODH (carbon monoxide dehydrogenase) and CLK2 (a protein kinase).
An increase of oxidised nucleotides activates DNA damage checkpoint pathway that regulates post-embryonic development in Caenorhabditis elegans.
Zhang-Akiyama et al., Kyoto, Japan. In Mutagenesis, 2014
This sensitivity was rescued by depletion of chk-2 and clk-2, suggesting that growth of the worms is regulated by the checkpoint pathway in response to the accumulation of oxidised nucleotides.
PHD3-dependent hydroxylation of HCLK2 promotes the DNA damage response.
Patterson et al., Chapel Hill, United States. In J Clin Invest, 2012
identification of HCLK2 as a substrate of PHD3 reveals the mechanism through which hypoxia inhibits the DDR, suggesting hydroxylation of HCLK2 is a potential therapeutic target for regulating the ATR/CHK1/p53 pathway
Differential effect of CLK SR Kinases on HIV-1 gene expression: potential novel targets for therapy.
Cochrane et al., Toronto, Canada. In Retrovirology, 2010
CLK1 Increases While CLK2 Decreases HIV-1 Gene Expression.
Phosphorylation of CLK2 at serine 34 and threonine 127 by AKT controls cell survival after ionizing radiation.
Jin et al., Seoul, South Korea. In J Biol Chem, 2010
AKT activation controls cell survival to ionizing radiation by phosphorylating CLK2, revealing an important regulatory mechanism required for promoting cell survival.
CK2 phospho-dependent binding of R2TP complex to TEL2 is essential for mTOR and SMG1 stability.
Boulton et al., London, United Kingdom. In Mol Cell, 2010
The CK2 phospho-dependent interaction between TEL2 and the R2TP complex affects phosphatidylinositol 3-kinase-related kinase functions and is essential for mTOR and SMG1 stability in vivo.
A genetic screen identifies the Triple T complex required for DNA damage signaling and ATM and ATR stability.
Elledge et al., Boston, United States. In Genes Dev, 2010
TTI1 and TTI2 exist in multiple complexes, including a 2-MDa complex with TEL2 (telomere maintenance 2), called the Triple T complex, and phosphoinositide-3-kinase-related protein kinases (PIKKs) such as ataxia telangiectasia-mutated (ATM).
Tel2: a common partner of PIK-related kinases and a link between DNA checkpoint and nutritional response?
Yanagida et al., Kyoto, Japan. In Genes Cells, 2007
A recent paper (Hayashi et al. 2007) in this issue of Genes to Cells shows that the fission yeast Schizosaccharomyces pombe Tel2, a homologue of mammalian/worm CLK2/Clk-2/Rad-5, physically interacts with all the phosphoinositide 3-kinase-related kinases (PIKKs) that include Rad3/Tel1 (ATR/ATM homologues), Tor1/Tor2 (TOR kinases) and Tra1/Tra2 (TRRAP homologues), raising the possibility that Tel2 family proteins link various PIKK-related cellular processes by interacting with PIKK family proteins.
HCLK2 is essential for the mammalian S-phase checkpoint and impacts on Chk1 stability.
Boulton et al., London, United Kingdom. In Nat Cell Biol, 2007
Here, we show that the human homologue of the Caenorhabditis elegans biological clock protein CLK-2 (HCLK2) associates with the S-phase checkpoint components ATR, ATRIP, claspin and Chk1.
Caenorhabditis elegans ABL-1 antagonizes p53-mediated germline apoptosis after ionizing irradiation.
Kolesnick et al., New York City, United States. In Nat Genet, 2004
Our findings delineate an apoptotic pathway antagonized by ABL-1, which requires sequentially the cell cycle checkpoint genes clk-2, hus-1 and mrt-2; the C. elegans p53 homolog, cep-1; and the genes encoding the components of the conserved apoptotic machinery, ced-3, ced-9 and egl-1.
Mechanisms of life span determination in Caenorhabditis elegans.
Braeckman et al., Gent, Belgium. In Neurobiol Aging, 1999
A different mechanism is specified by the clock genes clk-1, clk-2, clk-3 and gro-1, which regulate metabolic activity and the pace of many temporal processes including longevity.
Determination of life-span in Caenorhabditis elegans by four clock genes.
Hekimi et al., Montréal, Canada. In Science, 1996
Maternal-effect mutations in four genes--clk-1, clk-2, clk-3, and gro-1--interact genetically to determine both the duration of development and life-span.
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