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Cytoplasmic linker associated protein 1

CLASPs, such as CLASP1, are nonmotor microtubule-associated proteins that interact with CLIPs (e.g., CLIP170; MIM 179838). CLASP1 is involved in the regulation of microtubule dynamics at the kinetochore and throughout the spindle (Maiato et al., 2003 [PubMed 12837247]).[supplied by OMIM, Mar 2008] (from NCBI)
Top mentioned proteins: MAST, HAD, CLASP2, MAST205, OUT
Papers using sAST antibodies
Protein phosphatase 6 regulates mitotic spindle formation by controlling the T-loop phosphorylation state of Aurora A bound to its activator TPX2
Gruneberg Ulrike et al., In The Journal of Cell Biology, 2009
... ), rabbit anti-CLASP1 (Bethyl Laboratories, Inc.), CREST autoimmune ...
Papers on sAST
Germline mutations causing familial lung cancer.
Nagayasu et al., Nagasaki, Japan. In J Hum Genet, Oct 2015
We detected somatic 'candidate' mutations in multiple sporadic lung cancer samples; MAST1, CENPE, CACNB2 and LCT were the most promising candidate genes.
TPX2 phosphorylation maintains metaphase spindle length by regulating microtubule flux.
Zhang et al., Beijing, China. In J Cell Biol, Sep 2015
Interestingly, phosphorylation of TPX2 regulated its interaction with CLASP1 but not Kif2a.
Lead poisoning in Nile tilapia (Oreochromis niloticus): oxidant and antioxidant relationship.
Tanekhy, Rosetta, Egypt. In Environ Monit Assess, Apr 2015
On the other hand, insignificant decreases of sAST, sALT, urea, and creatinine in group fed on vitamin E and selenium, while increase in lead acetate intoxicated group.
Whole-exome sequencing points to considerable genetic heterogeneity of cerebral palsy.
MacLennan et al., Adelaide, Australia. In Mol Psychiatry, Feb 2015
Ten de novo mutations in three previously identified disease genes (TUBA1A (n=2), SCN8A (n=1) and KDM5C (n=1)) and in six novel candidate CP genes (AGAP1, JHDM1D, MAST1, NAA35, RFX2 and WIPI2) were predicted to be potentially pathogenic for CP.
Epitope Fingerprinting for Recognition of the Polyclonal Serum Autoantibodies of Alzheimer's Disease.
Ueira-Vieira et al., Uberlândia, Brazil. In Biomed Res Int, 2014
The putative antigens MAST1, Enah, MAO-A, X11/MINT1, HGF, SNX14, ARHGAP 11A, APC, and CENTG3, which have been associated with AD or have functions in neural tissue, may indicate possible therapeutic targets.
CLASPs link focal-adhesion-associated microtubule capture to localized exocytosis and adhesion site turnover.
Wittmann et al., San Francisco, United States. In Nat Cell Biol, 2014
We report that clustering of microtubule-associated CLASP1 and CLASP2 proteins around FAs temporally correlates with FA turnover.
CLASPs prevent irreversible multipolarity by ensuring spindle-pole resistance to traction forces during chromosome alignment.
Maiato et al., Porto, Portugal. In Nat Cell Biol, 2012
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.
Functionally recurrent rearrangements of the MAST kinase and Notch gene families in breast cancer.
Chinnaiyan et al., Ann Arbor, United States. In Nat Med, 2011
Overexpression of MAST1 or MAST2 gene fusions has a proliferative effect both in vitro and in vivo in breast cancer cell lines.
MAP4 and CLASP1 operate as a safety mechanism to maintain a stable spindle position in mitosis.
McAinsh et al., Coventry, United Kingdom. In Nat Cell Biol, 2011
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.
CLASP1, astrin and Kif2b form a molecular switch that regulates kinetochore-microtubule dynamics to promote mitotic progression and fidelity.
Compton et al., United States. In Embo J, 2010
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.
Golgi-derived CLASP-dependent microtubules control Golgi organization and polarized trafficking in motile cells.
Kaverina et al., Nashville, United States. In Nat Cell Biol, 2009
A role for microtubules that form at the Golgi membranes is identified in a manner dependent on the microtubule regulators CLASPs.
Human CLASP1 is an outer kinetochore component that regulates spindle microtubule dynamics.
Earnshaw et al., Edinburgh, United Kingdom. In Cell, 2003
Here, we show that CLASP1, a microtubule-associated protein, localizes preferentially near the plus ends of growing spindle microtubules and is also a component of a kinetochore region that we term the outer corona.
Antiplatelet therapy in acute cerebral ischemia.
Gross et al., Burlington, United States. In Stroke, 1999
Only 1 study, the Multicentre Acute Stroke Trial-Italy (MAST-I), entered patients within 6 hours of the ictus.
[Fibrinolysis in acute CVA: the current status].
Ferro, Coimbra, Portugal. In Acta Med Port, 1997
All three studies with Estreptoquinase--MAST-E, MAST-I and ASK--ended prematurely due to the high rates of mortality and intracranial haemorrhage observed in the group of patients treated with this drug.
Reliability of hemorrhagic transformation diagnosis in acute ischemic stroke.
Candelise et al., Milano, Italy. In Stroke, 1997
METHODS: Fifty 5-day CT scans of patients enrolled in the Multicenter Acute Stroke Trial-Italy (MAST-I) were reviewed independently by two neuroradiologists and one neurologist with CT training.
Thrombolytic therapy in the treatment of stroke.
del Zoppo, Los Angeles, United States. In Drugs, 1996
The Multicentre Acute Stroke Trial-Europe (MAST-E), the Australia Streptokinase (ASK), and the Multicentre Acute Stroke Trial-Italy (MAST-I) trials, which evaluated intravenous streptokinase 1.5 x 10(6) IU in patients with acute ischaemic stroke, were terminated prematurely because of excessive early mortality and symptomatic intracranial haemorrhage in streptokinase recipients compared with those treated with placebo.
Thrombolytic therapy. From myocardial to cerebral infarction. The MAST-I Group. Multicentre Acute Stroke Trial.
Maggioni et al., Milano, Italy. In Ital J Neurol Sci, 1996
Thrombolysis is proposed for the acute treatment of cerebral infarction as it is able to recanalize occluded arteries and thus potentially restore normal perfusion of the cerebral parenchyma, but the results concerning the efficacy of this treatment are still inconclusive.
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