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MASTL encodes a microtubule-associated serine/threonine kinase. Additionally we are shipping MASTL Kits (6) and MASTL Proteins (6) and many more products for this protein.
Showing 10 out of 80 products:
Human Polyclonal MASTL Primary Antibody for ICC, IF - ABIN4332787
Hégarat, Vesely, Vinod, Ocasio, Peter, Gannon, Oliver, Novák, Hochegger: PP2A/B55 and Fcp1 regulate Greatwall and Ensa dephosphorylation during mitotic exit. in PLoS genetics 2014
Human Polyclonal MASTL Primary Antibody for IHC, IHC (p) - ABIN439669
Della Monica, Visconti, Cervone, Serpico, Grieco: Fcp1 phosphatase controls Greatwall kinase to promote PP2A-B55 activation and mitotic progression. in eLife 2016
transient knockdown of MASTL correlates with a decrease in the expression of c-mpl (show MPL Antibodies) and GpIIb (show ITGA2B Antibodies), and reduction of circulating thrombocytes
Using mathematical modelling, this paper confirms that deactivation of MASTL is essential for mitotic exit.
these results established that precise control of MASTL is essential to couple DNA damage to mitosis through the rate of mitotic entry and APC (show APC Antibodies)/C activation.
Thus, GWL is a human oncoprotein that promotes the hyperactivation of AKT (show AKT1 Antibodies) via the degradation of its phosphatase, PHLPP (show PHLPP1 Antibodies), in human malignancies.
Thus, Fcp1 (show CTDP1 Antibodies) coordinates Cdk1 (show CDK1 Antibodies) and Gwl inactivation to derepress PP2A (show PPP2R4 Antibodies)-B55 (show MINK1 Antibodies), generating a dephosphorylation switch that drives mitosis progression.
Boolean modeling identifies Greatwall/MASTL as an important regulator in the AURKA (show AURKA Antibodies) network of neuroblastoma (show ARHGEF16 Antibodies).
Data show that siRNA knockdown of Forkhead box M1 (FOXM1 (show FOXM1 Antibodies)) or microtubule-associated serine/threonine kinase-like (MASTL) induces radiosensitivity in non-small cell lung cancer (NSCLC).
Mastl upregulation is involved in cancer progression and tumor recurrence after initial cancer therapy
data demonstrate that GWL acts in a pathway with PP2A (show PPP2R4 Antibodies) which is essential for prophase I exit and metaphase I microtubule assembly in mouse oocytes.
Taken together our results suggest a hierarchy of phosphatases coordinating Greatwall, Ensa (show ENSA Antibodies)/ARPP19 and Cdk (show CDK4 Antibodies) substrate dephosphorylation during mitotic exit.
Studies indicate that mutations in three different genes within the THC2 (show ANKRD26 Antibodies) locus have been associated with congenital thrombocytopenia, including a mutation in MASTL.
using in vitro dephosphorylation assays, we demonstrate that Mastl promotes persistent MPS1 phosphorylation by inhibiting PP2A (show PPP2R2B Antibodies)/B55 (show MINK1 Antibodies)-mediated MPS1 dephosphorylation rather than affecting Cdk1 (show CDK1 Antibodies) kinase activity. Our findings establish a key regulatory function of the Greatwall kinase/Mastl - PP2A (show PPP2R2B Antibodies)/B55 (show MINK1 Antibodies) pathway in preventing premature SAC (show ADCY10 Antibodies) silencing
Mastl is required for the timely activation of anaphase-promoting complex (show CDC26 Antibodies)/cyclosome to allow meiosis I exit and for the rapid rise of Cdk1 (show CDK1 Antibodies) activity.
Data show that Mastl (Greatwall)-null cells display mitotic collapse after nuclear envelope breakdown (NEB (show NEB Antibodies)) characterized by defective chromosome condensation and prometaphase arrest.
Data suggest Greatwall kinase (Gwl) associates with protein phosphatase 1 (show PPP1CB Antibodies) (PP1 (show PPYR1 Antibodies)), particularly PP1gamma subunit, which mediates dephosphorylation of Gwl Ser (show SIGLEC1 Antibodies)-883; consistent with mitotic activation of Gwl, its association with PP1 (show PPYR1 Antibodies) is disrupted in mitotic cells; subunits PPP1R3B (show PPP1R3B Antibodies) and PPP1R13L (show PPP1R13L Antibodies) associate with Gwl; thus, PPP1R3B (show PPP1R3B Antibodies) appears to act as cell cycle regulator (show CDKN2A Antibodies) in oocytes that functions by governing Gwl dephosphorylation.
Full dephosphorylation of Gwl results in complete inactivation of Arpp19 (show ARPP19 Antibodies) and ENSA (show ENSA Antibodies), and dephosphorylation of mitotic substrates. this feed-back loop irreversibly induces mitotic exit.
study provides evidence that PP1 (show PPYR1 Antibodies) targets the auto-phosphorylation site of Gwl, resulting in efficient Gwl inactivation; this step is necessary to facilitate subsequent complete dephosphorylation of Gwl by PP2A (show PPP2R2B Antibodies)-B55 (show MINK1 Antibodies)
we showed that the Gwl nuclear localization is indispensable for the biochemical function of Gwl in promoting mitotic entry.
PP2A (show PPP2R2B Antibodies)-B55delta, Greatwall and ARPP19 (show ARPP19 Antibodies) are not only required for entry into meiotic divisions, but are also pivotal effectors within the Cdk1 (show CDK1 Antibodies) auto-regulatory loop responsible for its independence with respect to the PKA-negative control.
Greatwall kinase and cyclin B-Cdk1 (show CDK1 Antibodies) are both critical constituents of M-phase-promoting factor.
inhibition of PP2A (show PPP2R2B Antibodies)-B55delta results from Ensa (show ENSA Antibodies), that is phosphorylated in mitosis by the protein kinase (show CSNK1D Antibodies) Greatwall; this converts Ensa (show ENSA Antibodies) into specific inhibitor of PP2A (show PPP2R2B Antibodies)-B55delta; this pathway represents a previously unknown element in mitosis control
3 phosphorylation sites (phosphosites) critical to Gwl activation (pT193, pT206, and pS883 in Xenopus laevis) located in evolutionarily conserved domains that differentiate Gwl from related kinases
Coordinated interplays between Plx1 (show PLK1 Antibodies) and Gwl are required for reactivation of these kinases from the G(2)/M DNA damage checkpoint and efficient checkpoint recovery.
mitotic entry and maintenance is not only mediated by the activation of cyclin B-Cdc2 but also by the regulation of PP2A (show PPP2R2B Antibodies) by GW
This gene encodes a microtubule-associated serine/threonine kinase. Mutations at this locus have been associated with autosomal dominant thrombocytopenia, also known as thrombocytopenia-2. Alternatively spliced transcript variants have been described for this locus.
microtubule-associated serine/threonine-protein kinase-like
, serine/threonine-protein kinase greatwall
, microtubule associated serine/threonine kinase-like
, greatwall protein kinase
, Serine/threonine-protein kinase greatwall
, Microtubule-associated serine/threonine-protein kinase-like