Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Automatic Gene Ontology annotation based on Rhea mapping
Combined Automated Annotation using Multiple IEA Methods
In vivo inactivation of MASTL kinase results in thrombocytopenia.
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Recombinant wild-type and E167D MASTL localize to the nucleus of transfected cells.
"The MASTL kinase protein, both wildtype and mutant forms, appears to localize within the nucleus of these BHK cells (Figure 6, Panels A & B) as determined by co-localization with the DNA counterstain, TO-PRO-3."
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Morpholino knockdown of mastl in zebrafish reduces circulating thrombocytes.
"A transient knockdown of MASTL in zebrafish results in deficiency of circulating thrombocytes."
Loss of human Greatwall results in G2 arrest and multiple mitotic defects due to deregulation of the cyclin B-Cdc2/PP2A balance.
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MASTL is the functional human orthologue of Greatwall and promotes mitotic entry and maintenance by inhibiting PP2A.
"Here we show that the functional human ortholog of Greatwall protein kinase (Gwl) is the microtubule-associated serine/threonine kinase-like protein, MAST-L."
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Complete depletion arrests human cells in G2; partial depletion causes mitotic defects and SAC failure that are rescued by PP2A co-depletion or okadaic acid.
"These phenotypes appear to be mediated by PP2A, as they could be rescued by either a double Gwl/PP2A knockdown or by the inhibition of this phosphatase with okadaic acid."
MASTL is the human orthologue of Greatwall kinase that facilitates mitotic entry, anaphase and cytokinesis.
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MASTL is nuclear in interphase and partly centrosomal in mitosis, when it is active.
"We found that MASTL localizes to the nucleus in interphase and re-localizes in part to centrosomes in mitosis, when it is active."
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MASTL depletion delays G2, slows chromosome condensation and causes anaphase and cytokinesis failure.
"Cells strongly depleted of MASTL by RNAi delay in G(2) phase and reveal slow chromosome condensation."
The substrate of Greatwall kinase, Arpp19, controls mitosis by inhibiting protein phosphatase 2A.
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Arpp19 and alpha-endosulfine are Greatwall substrates that, when phosphorylated, bind and inhibit PP2A.
"We identified cyclic adenosine monophosphate-regulated phosphoprotein 19 (Arpp19) and α-Endosulfine as two substrates of Gwl that, when phosphorylated by this kinase, associate with and inhibit PP2A, thus promoting mitotic entry."
Greatwall phosphorylates an inhibitor of protein phosphatase 2A that is essential for mitosis.
Cryo-EM structures of PP2A:B55-FAM122A and PP2A:B55-ARPP19.
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MASTL phosphorylates ARPP19 on Ser62, which is required for ARPP19 to inhibit PP2A:B55.
"The mechanisms by which these inhibitors block PP2A:B55 activity differ, as ARPP19 strictly requires phosphorylation by MASTL kinase to inhibit PP2A:B555,6, whereas FAM122A inhibits PP2A:B55 in a phosphorylation-independent manner7,8."
UniProt entry Q96GX5 (GWL_HUMAN)
Deep research summary for human MASTL (falcon)
MASTL (GWL) phosphorylates ARPP19
MASTL phosphorylates ENSA
MASTL Facilitates Mitotic Progression