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MASTL encodes a microtubule-associated serine/threonine kinase. Zusätzlich bieten wir Ihnen MASTL Kits (7) und MASTL Proteine (6) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 80 products:
Human Polyclonal MASTL Primary Antibody für 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 für 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 and GpIIb, and reduction of circulating thrombocytes
E2F8 (zeige E2F8 Antikörper) 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 Antikörper)/C activation.
Thus, GWL is a human oncoprotein that promotes the hyperactivation of AKT (zeige AKT1 Antikörper) via the degradation of its phosphatase, PHLPP (zeige PHLPP1 Antikörper), in human malignancies.
Thus, Fcp1 (zeige CTDP1 Antikörper) coordinates Cdk1 (zeige CDK1 Antikörper) and Gwl inactivation to derepress PP2A (zeige PPP2R4 Antikörper)-B55 (zeige MINK1 Antikörper), generating a dephosphorylation switch that drives mitosis progression.
Boolean modeling identifies Greatwall/MASTL as an important regulator in the AURKA (zeige AURKA Antikörper) network of neuroblastoma (zeige ARHGEF16 Antikörper).
Data show that siRNA knockdown of Forkhead box M1 (FOXM1 (zeige FOXM1 Antikörper)) 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 Antikörper) 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 Antikörper)/ARPP19 and Cdk (zeige CDK4 Antikörper) substrate dephosphorylation during mitotic exit.
using in vitro dephosphorylation assays, we demonstrate that Mastl promotes persistent MPS1 phosphorylation by inhibiting PP2A (zeige PPP2R2B Antikörper)/B55 (zeige MINK1 Antikörper)-mediated MPS1 dephosphorylation rather than affecting Cdk1 (zeige CDK1 Antikörper) kinase activity. Our findings establish a key regulatory function of the Greatwall kinase/Mastl - PP2A (zeige PPP2R2B Antikörper)/B55 (zeige MINK1 Antikörper) pathway in preventing premature SAC (zeige ADCY10 Antikörper) silencing
Mastl is required for the timely activation of anaphase-promoting complex (zeige CDC26 Antikörper)/cyclosome to allow meiosis I exit and for the rapid rise of Cdk1 (zeige CDK1 Antikörper) activity.
Data show that Mastl (Greatwall)-null cells display mitotic collapse after nuclear envelope breakdown (NEB (zeige NEB Antikörper)) characterized by defective chromosome condensation and prometaphase arrest.
Data suggest Greatwall kinase (Gwl) associates with protein phosphatase 1 (zeige PPP1CB Antikörper) (PP1), particularly PP1gamma subunit, which mediates dephosphorylation of Gwl Ser (zeige SIGLEC1 Antikörper)-883; consistent with mitotic activation of Gwl, its association with PP1 is disrupted in mitotic cells; subunits PPP1R3B (zeige PPP1R3B Antikörper) and PPP1R13L (zeige PPP1R13L Antikörper) associate with Gwl; thus, PPP1R3B (zeige PPP1R3B Antikörper) appears to act as cell cycle regulator (zeige CDKN2A Antikörper) in oocytes that functions by governing Gwl dephosphorylation.
Full dephosphorylation of Gwl results in complete inactivation of Arpp19 (zeige ARPP19 Antikörper) and ENSA (zeige ENSA Antikörper), 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 Antikörper)-B55 (zeige MINK1 Antikörper)
we showed that the Gwl nuclear localization is indispensable for the biochemical function of Gwl in promoting mitotic entry.
PP2A (zeige PPP2R2B Antikörper)-B55delta, Greatwall and ARPP19 (zeige ARPP19 Antikörper) are not only required for entry into meiotic divisions, but are also pivotal effectors within the Cdk1 (zeige CDK1 Antikörper) auto-regulatory loop responsible for its independence with respect to the PKA-negative control.
Greatwall kinase and cyclin B-Cdk1 (zeige CDK1 Antikörper) are both critical constituents of M-phase-promoting factor.
inhibition of PP2A (zeige PPP2R2B Antikörper)-B55delta results from Ensa (zeige ENSA Antikörper), that is phosphorylated in mitosis by the protein kinase (zeige CSNK1D Antikörper) Greatwall; this converts Ensa (zeige ENSA Antikörper) into specific inhibitor of PP2A (zeige PPP2R2B Antikörper)-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 (zeige PLK1 Antikörper) 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 Antikörper) 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