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    CLASP1 cytoplasmic linker associated protein 1 [ Homo sapiens (human) ]

    Gene ID: 23332, updated on 4-Aug-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Differential regulation of single microtubules and bundles by a three-protein module.

    Differential regulation of single microtubules and bundles by a three-protein module.
    Mani N, Jiang S, Neary AE, Wijeratne SS, Subramanian R., Free PMC Article

    09/11/2021
    Prickle1 localized to the membrane through its farnesyl moiety, and the membrane localization was necessary for Prickle1 to regulate migration, to bind to CLASPs and LL5beta, and to promote microtubule targeting of focal adhesions.

    Prickle1 promotes focal adhesion disassembly in cooperation with the CLASP-LL5β complex in migrating cells.
    Lim BC, Matsumoto S, Yamamoto H, Mizuno H, Kikuta J, Ishii M, Kikuchi A.

    08/5/2017
    catastrophe inhibition by SLAIN2 and CLASP1 supports mesenchymal cell shape in soft 3D matrices by enabling microtubules to perform a load-bearing function.

    Mesenchymal Cell Invasion Requires Cooperative Regulation of Persistent Microtubule Growth by SLAIN2 and CLASP1.
    Bouchet BP, Noordstra I, van Amersfoort M, Katrukha EA, Ammon YC, Ter Hoeve ND, Hodgson L, Dogterom M, Derksen PWB, Akhmanova A., Free PMC Article

    06/24/2017
    Acute silencing of CLASP1, a +TIP that participates in microtubule stabilization at the cell periphery, impairs trypomastigote internalization without diminishing the capacity for calcium-regulated lysosome exocytosis.

    Host microtubule plus-end binding protein CLASP1 influences sequential steps in the Trypanosoma cruzi infection process.
    Zhao X, Kumar P, Shah-Simpson S, Caradonna KL, Galjart N, Teygong C, Blader I, Wittmann T, Burleigh BA., Free PMC Article

    06/27/2015
    Propose that CLASPs couple microtubule organization, vesicle transport and cell interactions with the ECM, establishing a local secretion pathway that facilitates focal adhesion turnover by severing cell-matrix connections.

    CLASPs link focal-adhesion-associated microtubule capture to localized exocytosis and adhesion site turnover.
    Stehbens SJ, Paszek M, Pemble H, Ettinger A, Gierke S, Wittmann T., Free PMC Article

    08/9/2014
    our data suggest a model for mitotic spindle positioning in which RanGTP and CLASP1 cooperate to align the spindle along the long axis of the dividing cell.

    RanGTP and CLASP1 cooperate to position the mitotic spindle.
    Bird SL, Heald R, Weis K., Free PMC Article

    04/5/2014
    findings highlight the common mechanistic use of TOG domains in XMAP215 and CLASP families to regulate MT dynamics and suggest that differential TOG domain architecture may confer distinct functions to these critical cytoskeletal regulators

    A cryptic TOG domain with a distinct architecture underlies CLASP-dependent bipolar spindle formation.
    Leano JB, Rogers SL, Slep KC., Free PMC Article

    01/4/2014
    The epiblast epithelial status was maintained by anchoring microtubules to the basal cortex via CLIP1, a microtubule plus-end tracking protein, and Dystroglycan, a transmembrane protein that bridges the cytoskeleton and basement membrane (BM).

    Epiblast integrity requires CLASP and Dystroglycan-mediated microtubule anchoring to the basal cortex.
    Nakaya Y, Sukowati EW, Sheng G., Free PMC Article

    11/23/2013
    Data show that CENP-E-mediated traction forces on misaligned chromosomes are responsible for the irreversible loss of spindle-pole integrity in CLASP1/2-depleted cells.

    CLASPs prevent irreversible multipolarity by ensuring spindle-pole resistance to traction forces during chromosome alignment.
    Logarinho E, Maffini S, Barisic M, Marques A, Toso A, Meraldi P, Maiato H.

    05/12/2012
    Data show that the tau-related protein MAP4 and the microtubule rescue factor CLASP1 are essential for maintaining spindle position and the correct cell-division axis.

    MAP4 and CLASP1 operate as a safety mechanism to maintain a stable spindle position in mitosis.
    Samora CP, Mogessie B, Conway L, Ross JL, Straube A, McAinsh AD.

    12/10/2011
    Data show that CLASP1-astrin-Kif2b complex acts as a central switch at kinetochores that defines mitotic progression and promotes fidelity by temporally regulating kinetochore-microtuble attachments.

    CLASP1, astrin and Kif2b form a molecular switch that regulates kinetochore-microtubule dynamics to promote mitotic progression and fidelity.
    Manning AL, Bakhoum SF, Maffini S, Correia-Melo C, Maiato H, Compton DA., Free PMC Article

    11/27/2010
    Observational study of gene-disease association, gene-environment interaction, and pharmacogenomic / toxicogenomic. (HuGE Navigator)

    Variation at the NFATC2 locus increases the risk of thiazolidinedione-induced edema in the Diabetes REduction Assessment with ramipril and rosiglitazone Medication (DREAM) study.
    Bailey SD, Xie C, Do R, Montpetit A, Diaz R, Mohan V, Keavney B, Yusuf S, Gerstein HC, Engert JC, Anand S, DREAM investigators., Free PMC Article

    09/15/2010
    Observational study of gene-disease association. (HuGE Navigator)See all PubMed (2) articles

    Centrosome-related genes, genetic variation, and risk of breast cancer.
    Olson JE, Wang X, Pankratz VS, Fredericksen ZS, Vachon CM, Vierkant RA, Cerhan JR, Couch FJ.

    Gene-centric association signals for lipids and apolipoproteins identified via the HumanCVD BeadChip.
    Talmud PJ, Drenos F, Shah S, Shah T, Palmen J, Verzilli C, Gaunt TR, Pallas J, Lovering R, Li K, Casas JP, Sofat R, Kumari M, Rodriguez S, Johnson T, Newhouse SJ, Dominiczak A, Samani NJ, Caulfield M, Sever P, Stanton A, Shields DC, Padmanabhan S, Melander O, Hastie C, Delles C, Ebrahim S, Marmot MG, Smith GD, Lawlor DA, Munroe PB, Day IN, Kivimaki M, Whittaker J, Humphries SE, Hingorani AD, ASCOT investigators, NORDIL investigators, BRIGHT Consortium.

    06/30/2010
    Data propose that PRC1 forms a link between stabilization of CLASP1 association with central spindle microtubules and anti-parallel microtubule elongation.

    PRC1 cooperates with CLASP1 to organize central spindle plasticity in mitosis.
    Liu J, Wang Z, Jiang K, Zhang L, Zhao L, Hua S, Yan F, Yang Y, Wang D, Fu C, Ding X, Guo Z, Yao X., Free PMC Article

    01/21/2010
    A role for microtubules that form at the Golgi membranes is identified in a manner dependent on the microtubule regulators CLASPs.

    Golgi-derived CLASP-dependent microtubules control Golgi organization and polarized trafficking in motile cells.
    Miller PM, Folkmann AW, Maia AR, Efimova N, Efimov A, Kaverina I., Free PMC Article

    01/21/2010
    propose that CLASP1 and CLASP2 can mediate interactions between microtubule plus ends and the cell cortex and act as local rescue factors, possibly through forming a complex with EB1 at microtubule tips

    CLASP1 and CLASP2 bind to EB1 and regulate microtubule plus-end dynamics at the cell cortex.
    Mimori-Kiyosue Y, Grigoriev I, Lansbergen G, Sasaki H, Matsui C, Severin F, Galjart N, Grosveld F, Vorobjev I, Tsukita S, Akhmanova A., Free PMC Article

    01/21/2010
    A fusion protein of the putative microtubule-binding domain (1-662 out of 1289 residues) of hOrbit1 & GFP was transfected into human cells. The GFP-hOrbit1 N-terminal fragment binds to the newly formed microtubules rather than the pre-formed ones.

    Microtubule bundle formation and cell death induced by the human CLASP/Orbit N-terminal fragment.
    Aonuma M, Miyamoto M, Inoue YH, Tamai K, Sakai H, Kamasawa N, Matsukage A.

    01/21/2010
    These results suggest that CLASP1 is required at kinetochores to regulate the dynamic behavior of attached microtubules.

    How do kinetochores CLASP dynamic microtubules?
    Maiato H, Rieder CL, Earnshaw WC, Sunkel CE.

    01/21/2010
    CLASPs provide apparent stabilization of microtubules by locally reducing the amplitude of growth/shortening episodes at the microtubule ends.

    Mammalian CLASPs are required for mitotic spindle organization and kinetochore alignment.
    Mimori-Kiyosue Y, Grigoriev I, Sasaki H, Matsui C, Akhmanova A, Tsukita S, Vorobjev I.

    01/21/2010
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