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MASTL encodes a microtubule-associated serine/threonine kinase. Zusätzlich bieten wir Ihnen MASTL Antikörper (94) und MASTL Kits (8) und viele weitere Produktgruppen zu diesem Protein an.
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transient knockdown of MASTL correlates with a decrease in the expression of c-mpl and GpIIb, and reduction of circulating thrombocytes
E2F8 (zeige E2F8 Proteine) can shorten cisplatin induced G2/M arrest by promoting MASTL mediated mitotic progression in ER+ breast cancer cells, conferring drug resistance.
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 (zeige APC Proteine)/C activation.
Thus, GWL is a human oncoprotein that promotes the hyperactivation of AKT via the degradation of its phosphatase, PHLPP, in human malignancies.
Thus, Fcp1 (zeige CTDP1 Proteine) coordinates Cdk1 (zeige CDK1 Proteine) and Gwl inactivation to derepress PP2A (zeige PPP2R4 Proteine)-B55 (zeige MINK1 Proteine), generating a dephosphorylation switch that drives mitosis progression.
Boolean modeling identifies Greatwall/MASTL as an important regulator in the AURKA (zeige AURKA Proteine) network of neuroblastoma (zeige ARHGEF16 Proteine).
Data show that siRNA knockdown of Forkhead box M1 (FOXM1 (zeige FOXM1 Proteine)) 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 (zeige PPP2R4 Proteine) 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 (zeige ENSA Proteine)/ARPP19 and Cdk (zeige CDK4 Proteine) substrate dephosphorylation during mitotic exit.
using in vitro dephosphorylation assays, we demonstrate that Mastl promotes persistent MPS1 phosphorylation by inhibiting PP2A (zeige PPP2R2B Proteine)/B55 (zeige MINK1 Proteine)-mediated MPS1 dephosphorylation rather than affecting Cdk1 (zeige CDK1 Proteine) kinase activity. Our findings establish a key regulatory function of the Greatwall kinase/Mastl - PP2A (zeige PPP2R2B Proteine)/B55 (zeige MINK1 Proteine) pathway in preventing premature SAC (zeige ADCY10 Proteine) silencing
Mastl is required for the timely activation of anaphase-promoting complex (zeige CDC26 Proteine)/cyclosome to allow meiosis I exit and for the rapid rise of Cdk1 (zeige CDK1 Proteine) activity.
Data show that Mastl (Greatwall)-null cells display mitotic collapse after nuclear envelope breakdown (NEB) characterized by defective chromosome condensation and prometaphase arrest.
Data suggest Greatwall kinase (Gwl) associates with protein phosphatase 1 (zeige PPP1CB Proteine) (PP1), particularly PP1gamma subunit, which mediates dephosphorylation of Gwl Ser (zeige SIGLEC1 Proteine)-883; consistent with mitotic activation of Gwl, its association with PP1 is disrupted in mitotic cells; subunits PPP1R3B (zeige PPP1R3B Proteine) and PPP1R13L (zeige PPP1R13L Proteine) associate with Gwl; thus, PPP1R3B (zeige PPP1R3B Proteine) appears to act as cell cycle regulator in oocytes that functions by governing Gwl dephosphorylation.
Full dephosphorylation of Gwl results in complete inactivation of Arpp19 (zeige ARPP19 Proteine) and ENSA (zeige ENSA Proteine), and dephosphorylation of mitotic substrates. this feed-back loop irreversibly induces mitotic exit.
study provides evidence that PP1 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 (zeige PPP2R2B Proteine)-B55 (zeige MINK1 Proteine)
we showed that the Gwl nuclear localization is indispensable for the biochemical function of Gwl in promoting mitotic entry.
PP2A (zeige PPP2R2B Proteine)-B55delta, Greatwall and ARPP19 (zeige ARPP19 Proteine) are not only required for entry into meiotic divisions, but are also pivotal effectors within the Cdk1 (zeige CDK1 Proteine) auto-regulatory loop responsible for its independence with respect to the PKA-negative control.
Greatwall kinase and cyclin B-Cdk1 (zeige CDK1 Proteine) are both critical constituents of M-phase-promoting factor.
inhibition of PP2A (zeige PPP2R2B Proteine)-B55delta results from Ensa (zeige ENSA Proteine), that is phosphorylated in mitosis by the protein kinase (zeige CSNK1D Proteine) Greatwall; this converts Ensa (zeige ENSA Proteine) into specific inhibitor of PP2A (zeige PPP2R2B Proteine)-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 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 (zeige PPP2R2B Proteine) 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