The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.
You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.
We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.
We are interested in where in or outside the cell the gene product carries out its function.
We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.
Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.
Human MASTL encodes serine/threonine-protein kinase Greatwall (GWL; hGWL), UniProt Q96GX5. Its primary, experimentally established function is to phosphorylate ENSA at Ser67 and ARPP19 at Ser62. These phosphorylated endosulfines inhibit PP2A–B55, preventing premature dephosphorylation of CDK1 substrates and thereby enabling robust mitotic entry and maintenance. Following cyclin-B destruction, reversal of this pathway permits orderly mitotic exit. MASTL is therefore best annotated as an upstream inhibitor of a phosphatase rather than as a broad kinase acting directly on numerous mitotic proteins. (marzec2018theoncogenicfunctions pages 1-2, lorca2013thegreatwallkinase pages 4-5)
The protein is predominantly nuclear in interphase and becomes dispersed after nuclear-envelope breakdown. Outside canonical mitosis, evidence supports roles in platelet cytoskeletal regulation and a kinase-independent MASTL–MRTF-A/SRF pathway controlling adhesion and contractility. Cancer studies consistently nominate MASTL as a potential vulnerability, but the evidence remains preclinical: available inhibitors are micromolar tool compounds with off-target activity, and no MASTL-directed clinical trial was identified. (taskinen2020mastlpromotescell pages 1-2, taskinen2020mastlpromotescell pages 7-10, hurtado2018thrombocytopeniaassociatedmutationsin pages 1-3, ocasio2016afirstgeneration pages 8-11)
| Topic | Best-supported finding | Evidence type/system | Confidence/caveat |
|---|---|---|---|
| Identity | MASTL (UniProt Q96GX5) is the human functional ortholog of Greatwall kinase and an atypical AGC-family Ser/Thr kinase. It is not Drosophila MAST/Orbit or a mast-cell protein. It contains an unusual greater-than-500-aa insertion in its split kinase domain and lacks the PDZ domain typical of MAST1–4. (burgess2010lossofhuman pages 1-2, lorca2013thegreatwallkinase pages 4-5) | Sequence comparison, domain architecture, and functional rescue in Xenopus extracts | High. Identity and orthology are experimentally established; the historical name can produce misleading search matches. |
| Enzyme reaction and substrates | MASTL catalyzes ATP-dependent serine phosphorylation: ATP + ENSA/ARPP19 → ADP + phospho-ENSA/phospho-ARPP19. Canonical human sites are ENSA Ser67 and ARPP19 Ser62. Recombinant-domain assays measured Km values of 17.2 ± 2.4 μM for ATP and 1.6 ± 0.3 μM for ENSA. (marzec2018theoncogenicfunctions pages 1-2, lorca2013thegreatwallkinase pages 4-5, ocasio2016afirstgeneration pages 4-5) | Recombinant kinase assays, phosphosite mapping, egg extracts, and human-cell studies | High for ENSA-S67 and ARPP19-S62. Other proposed substrates may be context-specific. |
| PP2A–B55 mechanism | Phosphorylated ENSA/ARPP19 binds and inhibits PP2A–B55, opposing dephosphorylation of CDK1 substrates and supporting switch-like mitotic entry and maintenance. Cyclin-B destruction and restoration of phosphatase activity enable mitotic exit. (marzec2018theoncogenicfunctions pages 1-2, lorca2013thegreatwallkinase pages 4-5) | Biochemistry, phosphatase assays, Xenopus extracts, genetics, and human-cell depletion/rescue | High. This is MASTL's best-established primary function. |
| Localization | MASTL is predominantly nuclear during interphase, with a smaller cytoplasmic pool, and becomes broadly dispersed after nuclear-envelope breakdown during mitosis. Nuclear MASTL also associates with MRTF-A. (taskinen2020mastlpromotescell pages 1-2, taskinen2020mastlpromotescell pages 7-10) | Immunofluorescence and tagged-protein imaging in human epithelial and cancer cells | Moderate–high. Localization varies with cell-cycle stage, cell type, and expression system. |
| Loss phenotype | Complete human MASTL depletion causes G2 arrest; partial depletion causes prometaphase delay, premature mitotic-substrate dephosphorylation, spindle-checkpoint failure, aberrant mitotic exit, chromosome-segregation defects, and cytokinesis failure. PP2A inhibition or codepletion rescues key phenotypes. (burgess2010lossofhuman pages 1-2) | siRNA depletion and PP2A rescue experiments in human cells | High for cultured proliferating cells; severity depends on residual MASTL and experimental timing. |
| Platelets and E167D | Human E167D segregated with autosomal-dominant thrombocytopenia in one family. The corresponding mouse E166D allele caused reduced PP2A-associated dephosphorylation, cytoskeletal hyperphosphorylation, persistent pseudopods, abnormal platelet activation, and shortened platelet survival. Megakaryocyte-specific loss instead impaired maturation. (hurtado2018thrombocytopeniaassociatedmutationsin pages 1-3, hurtado2018thrombocytopeniaassociatedmutationsin pages 7-10) | Human genetics, knock-in and conditional-knockout mice, and platelet phosphoproteomics | Moderate–high mechanistically, but limited clinically. Human evidence comes from a rare family, and nearby genes can also cause thrombocytopenia. |
| Kinase-independent MRTF-A role | MASTL binds MRTF-A, promotes its nuclear retention and MRTF-A/SRF transcription, and supports contractility-associated genes including TPM4, VCL, MYH10, and ARHGEF2. Kinase-dead G44S rescued spreading and SRF-related phenotypes, supporting a noncatalytic role. (taskinen2020mastlpromotescell pages 1-2, taskinen2020mastlpromotescell pages 7-10) | Knockdown/rescue, co-immunoprecipitation, FLIP, transcriptomics, proteomics, and motility assays | Moderate. Strong cell-based evidence, but physiological importance and interaction structure remain incompletely validated in vivo. |
| 2023/2024 structural advance | Cryo-EM structures of PP2A–B55 bound to MASTL-thiophosphorylated ARPP19 resolved the complex at 2.77 Å. ARPP19 makes multiple B55 contacts while phospho-Ser62 enters the PP2A catalytic site; phosphorylated ARPP19 inhibited PP2A–B55 about 250-fold more potently than FAM122A. Published online 20 December 2023 and in Nature on 4 January 2024. (padi2024cryoemstructuresof pages 1-2, padi2024cryoemstructuresof pages 3-4, padi2024cryoemstructuresof pages 6-7) | Cryo-EM, NMR, binding assays, mutagenesis, and phosphatase assays | High for the downstream mechanism. This is a PP2A–B55–ARPP19 structure, not a structure of full-length MASTL. |
| 2024 gastric-cancer study | ABPP identified MASTL among HSP90-regulated kinases in sensitive gastric-cancer lines. MASTL knockdown reduced clonogenic growth, migration, and invasion; global proteomics implicated NEDD4-1 as a downstream mediator. The study identified 83, 64, 68, and 67 kinases in AGS, SNU484, SNU601, and MKN74 cells, respectively. (choi2024activitybasedproteinprofiling pages 7-11, choi2024activitybasedproteinprofiling pages 1-2, choi2024activitybasedproteinprofiling pages 4-5, choi2024activitybasedproteinprofiling pages 11-13) | ATP-probe ABPP, LC–MS/MS proteomics, siRNA, public tumor datasets, and cell assays | Moderate and preclinical. NEDD4-1 was not established as a direct MASTL substrate; no animal efficacy or patient intervention was reported. |
| GKI-1 and clinical status | First-generation inhibitor GKI-1 inhibited full-length human MASTL at about 4.9 μM and a minimal kinase domain at about 2.5 μM. At 25–50 μM in HeLa cells it reduced ENSA-S67 phosphorylation and reproduced MASTL-loss phenotypes, but it had AGC-kinase off-targets, including ROCK1 at about 11 μM. No MASTL-directed clinical trial was identified. (ocasio2016afirstgeneration pages 4-5, ocasio2016afirstgeneration pages 8-11, ocasio2016afirstgeneration pages 1-2) | Recombinant and immunoprecipitated kinase assays, structural studies, 50-kinase profiling, and human-cell imaging | High as a tool-compound result; low clinical maturity because potency and selectivity are insufficient for clinical validation. |
Table: Concise evidence map for human MASTL/Greatwall kinase Q96GX5, covering its verified identity, core biochemical mechanism, localization, disease evidence, recent structural and cancer findings, and therapeutic maturity.
The requested symbol matches the supplied identity: MASTL means microtubule-associated serine/threonine kinase-like and encodes the human Greatwall kinase. Burgess and colleagues experimentally established MASTL as the functional human orthologue of Greatwall through sequence comparison and functional rescue in Xenopus extracts. Human MASTL showed reported sequence homology of 50.2% to Drosophila Greatwall and 65.7% to Xenopus Greatwall. (burgess2010lossofhuman pages 1-2)
The organism is Homo sapiens. The retrieved human literature uses MASTL, MAST-L, Greatwall, GWL and hGWL for this protein. The supplied alias THC2 reflects its historical association with autosomal-dominant thrombocytopenia.
MASTL is an atypical AGC-family serine/threonine kinase. Its catalytic domain has the conventional protein-kinase two-lobe fold but is interrupted by an unusual insertion of more than 500 amino acids between kinase subdomains VII and VIII. A structural minimal-domain study identified AGC-associated C-terminal regulatory features, including C-lobe anchor, C-lobe tether and active-site tether elements; the minimal kinase domain retained ENSA-directed activity. (lorca2013thegreatwallkinase pages 4-5, ocasio2016afirstgeneration pages 4-5)
Despite its historical name, MASTL is not simply another member of the MAST1–MAST4 scaffold-kinase group: it has little similarity to MAST1 outside the catalytic core and lacks their characteristic C-terminal PDZ domain. This agrees with the supplied protein-kinase, AGC-kinase-C and MASTL-specific domain annotations. (burgess2010lossofhuman pages 1-2)
This report excludes three recurrent false matches:
The target identity is therefore sufficiently verified to proceed.
MASTL is an ATP-dependent protein serine kinase:
ATP + ENSA/ARPP19 → ADP + phospho-ENSA/phospho-ARPP19
The best-established human substrate sites are:
Both sites lie in a conserved endosulfine sequence context. Their phosphorylation converts ENSA and ARPP19 into potent inhibitors of PP2A holoenzymes containing a B55 regulatory subunit. (marzec2018theoncogenicfunctions pages 1-2, lorca2013thegreatwallkinase pages 4-5)
A recombinant human minimal-domain study reported an ATP-hydrolysis Km of 17.2 ± 2.4 μM and kcat of 10.4 ± 0.48 s⁻¹; using ENSA as substrate, the reported Km was 1.6 ± 0.3 μM and kcat 0.20 ± 0.01 s⁻¹. These values establish direct catalytic activity, although kinetics from a modified minimal construct should not be assumed to reproduce full-length MASTL in cells exactly. (ocasio2016afirstgeneration pages 4-5)
ENSA and ARPP19 are the canonical, high-confidence physiological substrates. The functional specificity is unusually narrow compared with many mitotic kinases: MASTL principally regulates the mitotic phosphoproteome indirectly by inhibiting PP2A–B55 rather than by phosphorylating hundreds of mitotic structural proteins itself. Other candidate substrates reported in particular contexts—including cytoskeletal proteins or cancer-specific candidates—require stronger independent validation and should not replace ENSA/ARPP19 in the primary annotation. (conway2020kinaseindependentfunctionsof pages 1-5, conway2020kinaseindependentfunctionsof pages 5-6)
At the G2/M transition, rising cyclin-B–CDK1 activity activates a positive-feedback network that includes MASTL. Active MASTL phosphorylates ENSA and ARPP19; phospho-ENSA/phospho-ARPP19 then inhibit PP2A–B55, the phosphatase that otherwise removes many CDK1-generated mitotic phosphates. This creates a switch-like state in which kinase output rises while the opposing phosphatase is suppressed. (marzec2018theoncogenicfunctions pages 1-2, lorca2013thegreatwallkinase pages 4-5)
Consequently, MASTL supports nuclear-envelope breakdown, chromosome condensation, spindle formation, spindle-checkpoint signaling, chromosome segregation and cytokinesis by preserving phosphorylation rather than by serving as a spindle structural component. Complete depletion in human cells causes G2 arrest. Partial depletion produces dose-dependent prometaphase delay, premature mitotic-substrate dephosphorylation, spindle-assembly-checkpoint failure, aberrant mitotic exit and cytokinesis defects. Codepletion or pharmacological inhibition of PP2A rescues important phenotypes, strongly supporting pathway causality. (burgess2010lossofhuman pages 1-2)
At mitotic exit, APC/C-mediated cyclin-B destruction lowers CDK1 activity. PP1 activation and MASTL dephosphorylation reduce MASTL signaling, after which PP2A–B55 reactivates and dephosphorylates mitotic substrates. Thus, MASTL helps establish mitosis, whereas turning it off helps order mitotic exit. (marzec2018theoncogenicfunctions pages 1-2)
A major recent advance was the PP2A–B55–ARPP19 cryo-EM study by Padi et al., published online 20 December 2023 and in Nature on 4 January 2024: https://doi.org/10.1038/s41586-023-06870-3. The authors generated MASTL-thiophosphorylated ARPP19 and solved the PP2A–B55 complex at 2.77 Å global resolution. (padi2024cryoemstructuresof pages 1-2, padi2024cryoemstructuresof pages 3-4)
ARPP19 engages several surfaces on B55 and the PP2A catalytic subunit; phospho/thiophospho-Ser62 projects into the catalytic site. The work explains the “unfair competition” behavior of phospho-endosulfines: they bind as substrates but are dephosphorylated slowly, occupying and inhibiting the phosphatase long enough to protect the broader mitotic phosphoproteome. Thiophosphorylated ARPP19 inhibited PP2A–B55 approximately 250-fold more potently than FAM122A in the reported assays. (padi2024cryoemstructuresof pages 1-2, padi2024cryoemstructuresof pages 6-7)
This structure is not a structure of full-length MASTL. Rather, it supplies high-resolution evidence for the downstream molecular consequence of MASTL catalysis.
Human MASTL is predominantly nuclear during interphase, although a reproducible cytoplasmic pool is present. During mitotic entry and nuclear-envelope breakdown, it becomes distributed through the mitotic cell, allowing the MASTL–endosulfine pathway to suppress PP2A–B55 across relevant compartments. (burgess2010lossofhuman pages 1-2, taskinen2020mastlpromotescell pages 7-10)
Nuclear localization also fits its noncanonical interaction with MRTF-A. In mammary epithelial and breast-cancer cells, MASTL associated with MRTF-A and promoted its nuclear retention and SRF-dependent transcription. Localization should therefore be annotated as cell-cycle dependent rather than as exclusively nuclear or cytoplasmic. (taskinen2020mastlpromotescell pages 1-2, taskinen2020mastlpromotescell pages 7-10)
Human MASTL E167D was reported to segregate with nonsyndromic autosomal-dominant thrombocytopenia in one family. A corresponding mouse E166D knock-in did not behave as a simple loss-of-function allele; it produced increased phosphorylation consistent with reduced PP2A activity, aberrant platelet activation, hyperstabilized pseudopods, defective actin remodeling and reduced platelet survival. In contrast, megakaryocyte-specific Mastl deletion impaired megakaryocyte maturation. (hurtado2018thrombocytopeniaassociatedmutationsin pages 1-3, hurtado2018thrombocytopeniaassociatedmutationsin pages 7-10)
Platelet phosphoproteomics identified 42 hyperphosphorylated sites in 43 proteins shared between resting and three-minute thrombin-activated mutant platelets at the stated log2-fold-change threshold. Focal-adhesion and actin-cytoskeleton pathways were prominent. Inhibition of PKA, PKC or AMPK partially rescued cytoskeletal abnormalities, connecting altered PP2A-controlled phosphorylation to the phenotype. (hurtado2018thrombocytopeniaassociatedmutationsin pages 7-10)
The clinical inference requires caution. The human evidence derives from a rare pedigree, and nearby ANKRD26 and ACBD5 variants can also cause inherited thrombocytopenia. Open Targets lists MASTL–autosomal thrombocytopenia as an association, but database scores and high-throughput associations are not substitutes for mechanistic evidence. (OpenTargets Search: -MASTL, hurtado2018thrombocytopeniaassociatedmutationsin pages 1-3)
Taskinen et al. reported in Journal of Cell Biology on 20 April 2020 that MASTL supports actomyosin contractility, migration and invasion through a kinase-independent mechanism: https://doi.org/10.1083/jcb.201906204. MASTL depletion increased spreading and reduced contractile stress fibers and motility in mammary epithelial and breast-cancer cells. Transcriptome analysis identified 139 altered transcripts at 24 hours and 247 at 48 hours, with approximately 75% downregulated; the two time points correlated at r = 0.73, P < 2.2 × 10⁻¹⁶. (taskinen2020mastlpromotescell pages 1-2)
Mechanistically, MASTL associated with MRTF-A and promoted its nuclear retention and MRTF-A/SRF transcription of cytoskeletal genes including TPM4, VCL, MYH10 and ARHGEF2. Kinase-dead G44S MASTL rescued cell-spreading and SRF phenotypes, supporting a noncatalytic scaffolding or retention function. This is persuasive cell-based evidence but remains less established physiologically than the ENSA/ARPP19–PP2A–B55 pathway. (taskinen2020mastlpromotescell pages 1-2, taskinen2020mastlpromotescell pages 7-10)
MASTL overexpression or pathway deregulation has been associated with chromosome instability, proliferation, invasion, metastasis, therapy resistance and poor outcome in several cancers. The mechanistic rationale is strong: excessive MASTL can suppress PP2A–B55 and distort the balance between mitotic phosphorylation and dephosphorylation. Reviews also note proposed connections to AKT/mTOR, Wnt/β-catenin and DNA-damage recovery, but many such links are context dependent and do not always identify a direct MASTL substrate. (conway2020kinaseindependentfunctionsof pages 1-5, marzec2018theoncogenicfunctions pages 1-2, conway2020kinaseindependentfunctionsof pages 5-6)
A 2023 prostate-cancer study, summarized in a 2024 Nature Reviews Urology review, implicated MASTL-dependent adaptation to chromosomal instability in aggressive, therapy-refractory disease. This supports target prioritization but remains preclinical rather than a validated biomarker or treatment standard.
Choi et al., accepted 8 August 2024, combined ATP-probe activity-based protein profiling with global proteomics in gastric-cancer cells: https://doi.org/10.1186/s12964-024-01783-8. They profiled two HSP90-inhibitor-sensitive lines, AGS and SNU484, and two resistant lines, SNU601 and MKN74. The study identified 83, 64, 68 and 67 kinases, respectively, and defined an HSP90-regulated candidate set containing MASTL, STK11, CHEK1 and MET. MASTL knockdown reduced clonogenic proliferation, migration and invasion. (choi2024activitybasedproteinprofiling pages 1-2, choi2024activitybasedproteinprofiling pages 4-5)
Global proteomics nominated the ubiquitin ligase NEDD4-1 as a downstream mediator; NEDD4-1 knockdown phenocopied reduced proliferation, migration and invasion. MASTL and ANLN expression correlated in gastric tumors at r = 0.69, P = 9.1 × 10⁻⁵⁹. However, neither NEDD4-1 nor ANLN was established as a direct MASTL substrate, and the authors explicitly stated that phosphoproteomics would be required to identify direct substrates. The evidence is therefore target-discovery evidence, not proof of a clinically actionable MASTL–NEDD4-1 pathway. (choi2024activitybasedproteinprofiling pages 7-11, choi2024activitybasedproteinprofiling pages 11-13)
The first-generation inhibitor GKI-1 was reported in 2016: https://doi.org/10.18632/oncotarget.11511. It inhibited full-length human MASTL at approximately 4.9 μM and a minimal domain at approximately 2.5 μM. In nocodazole-treated HeLa cells, 25 μM GKI-1 reduced phospho-ENSA signal about twofold, while 50 μM approached the effect of MASTL depletion and induced mitotic and cytokinesis phenotypes. (ocasio2016afirstgeneration pages 8-11, ocasio2016afirstgeneration pages 1-2)
GKI-1 is not a clinically suitable selective inhibitor: it inhibited ROCK1 at approximately 11.3 ± 3.4 μM and showed additional AGC-family off-target activity in a 50-kinase panel. It is best regarded as a chemical starting point or tool compound. Computational work in 2024 proposed potentially discriminating pockets across MAST-family kinase models, but virtual pocket transfer is hypothesis generation, not experimental inhibitor validation.
No relevant MASTL-directed interventional clinical trial was retrieved. Current real-world applications are therefore limited to research use: mechanistic cell-cycle studies, phospho-ENSA/ARPP19 pathway readouts, inherited-thrombocytopenia investigation and preclinical cancer target validation.
Established with high confidence: human identity; atypical AGC-kinase architecture; ENSA-Ser67 and ARPP19-Ser62 phosphorylation; PP2A–B55 inhibition; control of G2/M and mitotic phosphorylation; predominantly nuclear interphase localization; severe cell-cycle defects after depletion.
Supported but context dependent: platelet cytoskeletal regulation, MRTF-A/SRF signaling, DNA-damage recovery and cancer-cell migration/invasion.
Emerging or insufficiently validated: additional direct substrates, universal oncogenic signaling through AKT or Wnt, use as a prognostic biomarker across tumor types, and therapeutic efficacy of MASTL inhibition in patients.
The most defensible functional annotation for human MASTL/Q96GX5 is: an atypical AGC-family serine/threonine kinase that phosphorylates ENSA-Ser67 and ARPP19-Ser62 to inhibit PP2A–B55, thereby preserving CDK1-dependent phosphorylation during mitotic entry and maintenance. It acts predominantly from the nucleus before nuclear-envelope breakdown and throughout the mitotic cell thereafter. Platelet and MRTF-A findings broaden its biology beyond proliferation, but these roles are secondary to the canonical MASTL–endosulfine–PP2A axis. Recent structural work has clarified the downstream inhibition mechanism at near-atomic resolution, while 2024 cancer proteomics strengthened the rationale for therapeutic targeting. Nevertheless, clinical translation remains immature because selective, potent inhibitors and human intervention data are lacking.
References
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(OpenTargets Search: -MASTL): Open Targets Query (-MASTL, 5 results). Buniello, A. et al. (2025). Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery. Nucleic Acids Research.