anti-Microtubule Associated serine/threonine Kinase-Like (MASTL) Antibodies

Zebrafish Microtubule Associated serine/threonine Kinase-Like (MASTL) interaction partners

1. transient knockdown of MASTL correlates with a decrease in the expression of c-mpl and GpIIb, and reduction of circulating thrombocytes

Human Microtubule Associated serine/threonine Kinase-Like (MASTL) interaction partners

1. Data show that MASTL expression increases in colon cancer (CC) across all cancer stages. Also, increased levels of MASTL associated with high-risk disease and poor prognosis. Further, its silencing induced cell cycle arrest and apoptosis in vitro and inhibited xenograft-tumor growth. Functional analysis revealed that MASTL expression facilitates CC progression and chemoresistance by promoting the beta-catenin/Wnt signa...

2. MASTL overexpression contributes to chromosome instability and metastasis, thereby decreasing breast cancer patient survival.

3. E2F8 can shorten cisplatin induced G2/M arrest by promoting MASTL mediated mitotic progression in ER+ breast cancer cells, conferring drug resistance.

4. Using mathematical modelling, this paper confirms that deactivation of MASTL is essential for mitotic exit.

5. these results established that precise control of MASTL is essential to couple DNA damage to mitosis through the rate of mitotic entry and APC/C activation.

6. Thus, GWL is a human oncoprotein that promotes the hyperactivation of AKT via the degradation of its phosphatase, PHLPP, in human malignancies.

7. Thus, Fcp1 coordinates Cdk1 and Gwl inactivation to derepress PP2A-B55, generating a dephosphorylation switch that drives mitosis progression.

8. Boolean modeling identifies Greatwall/MASTL as an important regulator in the AURKA network of neuroblastoma.

9. Data show that siRNA knockdown of Forkhead box M1 (FOXM1) or microtubule-associated serine/threonine kinase-like (MASTL) induces radiosensitivity in non-small cell lung cancer (NSCLC).

10. Mastl upregulation is involved in cancer progression and tumor recurrence after initial cancer therapy

11. 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.

12. Taken together our results suggest a hierarchy of phosphatases coordinating Greatwall, Ensa/ARPP19 and Cdk substrate dephosphorylation during mitotic exit.

13. Studies indicate that mutations in three different genes within the THC2 locus have been associated with congenital thrombocytopenia, including a mutation in MASTL.

14. results identify Gwl as a member of the AGC family of kinases that appears to be regulated by unique mechanisms and that differs from the other members of this family

15. MASTL enhances cyclin B1-Cdk1-dependent mitotic phosphorylation events, directing mitotic entry, anaphase and cytokinesis in human cells.

16. A paper that narrows the identity of the gene for autosomal dominant thrombocytopenia (THC2) to FLJ14813. The mutation is present in all affected people across three generations while is absent in unaffected family members & 94 random blood donors.

Mouse (Murine) Microtubule Associated serine/threonine Kinase-Like (MASTL) interaction partners

1. Findings reveal the role of RSK in mouse oocytes, showing that the RSK-MASTL pathway allows mammalian-specific prolonged meiotic exit and ensures the faithful conversion from sperm to paternal pronuclei.

2. using in vitro dephosphorylation assays, we demonstrate that Mastl promotes persistent MPS1 phosphorylation by inhibiting PP2A/B55-mediated MPS1 dephosphorylation rather than affecting Cdk1 kinase activity. Our findings establish a key regulatory function of the Greatwall kinase/Mastl - PP2A/B55 pathway in preventing premature SAC silencing

3. Mastl is required for the timely activation of anaphase-promoting complex/cyclosome to allow meiosis I exit and for the rapid rise of Cdk1 activity.

4. Data show that Mastl (Greatwall)-null cells display mitotic collapse after nuclear envelope breakdown (NEB) characterized by defective chromosome condensation and prometaphase arrest.

Xenopus laevis Microtubule Associated serine/threonine Kinase-Like (MASTL) interaction partners

1. Data suggest Greatwall kinase (Gwl) associates with protein phosphatase 1 (PP1), particularly PP1gamma subunit, which mediates dephosphorylation of Gwl Ser-883; consistent with mitotic activation of Gwl, its association with PP1 is disrupted in mitotic cells; subunits PPP1R3B and PPP1R13L associate with Gwl; thus, PPP1R3B appears to act as cell cycle regulator in oocytes that functions by governing Gwl dephosphorylation.

2. Full dephosphorylation of Gwl results in complete inactivation of Arpp19 and ENSA, and dephosphorylation of mitotic substrates. this feed-back loop irreversibly induces mitotic exit.

3. 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-B55

4. we showed that the Gwl nuclear localization is indispensable for the biochemical function of Gwl in promoting mitotic entry.

5. PP2A-B55delta, Greatwall and ARPP19 are not only required for entry into meiotic divisions, but are also pivotal effectors within the Cdk1 auto-regulatory loop responsible for its independence with respect to the PKA-negative control.

6. Greatwall kinase and cyclin B-Cdk1 are both critical constituents of M-phase-promoting factor.

7. 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

8. 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

9. 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.

10. mitotic entry and maintenance is not only mediated by the activation of cyclin B-Cdc2 but also by the regulation of PP2A by GW

11. [review] The kinase Greatwall phosphorylates small protein ARPP-19 and converts it into a potent antimitotic PP2A inhibitor.