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MASTL encodes a microtubule-associated serine/threonine kinase. Additionally we are shipping MASTL Antibodies (82) and MASTL Proteins (6) and many more products for this protein.
Showing 6 out of 6 products:
transient knockdown of MASTL correlates with a decrease in the expression of c-mpl and GpIIb, 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 ELISA Kits)/C activation.
Thus, GWL is a human oncoprotein that promotes the hyperactivation of AKT (show AKT1 ELISA Kits) via the degradation of its phosphatase, PHLPP (show PHLPP1 ELISA Kits), in human malignancies.
Thus, Fcp1 (show CTDP1 ELISA Kits) coordinates Cdk1 (show CDK1 ELISA Kits) and Gwl inactivation to derepress PP2A (show PPP2R4 ELISA Kits)-B55 (show MINK1 ELISA Kits), generating a dephosphorylation switch that drives mitosis progression.
Boolean modeling identifies Greatwall/MASTL as an important regulator in the AURKA (show AURKA ELISA Kits) network of neuroblastoma (show ARHGEF16 ELISA Kits).
Data show that siRNA knockdown of Forkhead box M1 (FOXM1 (show FOXM1 ELISA Kits)) 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 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 ELISA Kits)/ARPP19 (show ARPP19 ELISA Kits) and Cdk (show CDK4 ELISA Kits) substrate dephosphorylation during mitotic exit.
Studies indicate that mutations in three different genes within the THC2 (show ANKRD26 ELISA Kits) locus have been associated with congenital thrombocytopenia, including a mutation in MASTL.
Mastl is required for the timely activation of anaphase-promoting complex (show CDC26 ELISA Kits)/cyclosome to allow meiosis I exit and for the rapid rise of Cdk1 (show CDK1 ELISA Kits) activity.
Data show that Mastl (Greatwall)-null cells display mitotic collapse after nuclear envelope breakdown (NEB (show NEB ELISA Kits)) characterized by defective chromosome condensation and prometaphase arrest.
Full dephosphorylation of Gwl results in complete inactivation of Arpp19 and ENSA (show ENSA ELISA Kits), and dephosphorylation of mitotic substrates. this feed-back loop irreversibly induces mitotic exit.
study provides evidence that PP1 (show PPYR1 ELISA Kits) 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-B55 (show MINK1 ELISA Kits)
we showed that the Gwl nuclear localization is indispensable for the biochemical function of Gwl in promoting mitotic entry.
PP2A-B55delta, Greatwall and ARPP19 are not only required for entry into meiotic divisions, but are also pivotal effectors within the Cdk1 (show CDK1 ELISA Kits) auto-regulatory loop responsible for its independence with respect to the PKA-negative control.
Greatwall kinase and cyclin B-Cdk1 (show CDK1 ELISA Kits) are both critical constituents of M-phase-promoting factor.
inhibition of PP2A-B55delta results from Ensa, that is phosphorylated in mitosis by the protein kinase Greatwall; this converts Ensa into specific inhibitor of PP2A-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 ELISA Kits) 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 by GW
[review] The kinase Greatwall phosphorylates small protein ARPP-19 and converts it into a potent antimitotic PP2A inhibitor.
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