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this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.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.
The requested identity is internally consistent: MYL10 (human Ensembl target ENSG00000106436; UniProt Q9BUA6; aliases MYLC2PL/PLRLC) is myosin regulatory light chain 10, not the heavy-chain gene MYH10, a myosin-light-chain kinase (MYLK), or the better-characterized RLC paralogs MYL2, MYL9, or MYL12A/B. Literature independently places MYL10 in the human regulatory-light-chain family; its EF-hand/Myosin_RLC annotation is therefore coherent with the supplied UniProt record. Foundational PLRLC experiments, however, were predominantly performed in mice rather than with purified human Q9BUA6. (oltz1992anovelregulatory pages 5-7, oltz1992anovelregulatory pages 2-3, heissler2014myosinlightchains pages 4-5)
The most defensible primary annotation is: MYL10 is a nonenzymatic, calmodulin-superfamily regulatory light-chain protein predicted to associate with a myosin heavy-chain neck/lever-arm region and modulate or stabilize actomyosin mechanics. It is not itself an ATPase, kinase, transporter, or receptor. Critically, the native human heavy-chain partner, phosphorylation-dependent regulation, calcium affinity, and precise intracellular localization have not been established by MYL10-specific biochemical or imaging experiments in the retrieved literature. Thus, “myosin structural/regulatory subunit” is well-supported at the family level, whereas a precise motor complex or signaling mechanism remains unverified. (heissler2014myosinlightchains pages 4-5)
The 1992 PLRLC study identified a distinct regulatory-MLC-2-related locus with multiple transcripts and showed related sequences in human DNA. Its coding region was 79% amino-acid identical to rat cardiac MLC-2, or 87% when conservative substitutions were included. Southern analysis distinguished PLRLC from other RLC genes. Later expert review explicitly listed MYL10 among the human RLC genes, alongside MYL2, MYL5, MYL7, MYL9, MYL11, MYL12A, and MYL12B. (oltz1992anovelregulatory pages 5-7, heissler2014myosinlightchains pages 4-5)
The supplied InterPro/Pfam annotations—EF-hand domain pair, EF-hand calcium-binding-site signature, EF-hand domain, Myosin_RLC, and EF-hand_6—fit this family assignment. RLCs are calmodulin-like proteins with four EF-hand-derived motifs, but expert review cautions that such motifs may be degenerate and need not retain effective calcium binding. Consequently, the domain annotation supports fold and ancestry but does not by itself prove that human MYL10 binds Ca²⁺ under physiological conditions. (heissler2014myosinlightchains pages 4-5)
Literature involving nonhuman “myl10,” especially fish muscle genes, was not treated as direct evidence for human Q9BUA6. Likewise, results for MYL2, MYL9, or MYL12 cannot be assigned to MYL10 merely because all are RLCs.
Myosin RLCs generally bind the α-helical neck of a myosin heavy chain, stabilize the lever arm, and can tune motor assembly, force production, ATPase–mechanical coupling, or filament organization. On that basis, MYL10 is best classified as a myosin-associated structural/regulatory subunit. Its relevant “substrate,” in the enzymatic sense, is therefore none; the likely binding substrate is a myosin-heavy-chain IQ/neck region, but the native human partner has not been identified directly. (heissler2014myosinlightchains pages 4-5)
Claims that MYL10 is phosphorylated by MLCK, activates a particular myosin-II isoform, or directly binds calcium should presently be labeled hypotheses extrapolated from other RLCs. No retrieved study supplied purified-human-MYL10 kinase assays, phosphosite stoichiometry, calcium-binding constants, myosin-reconstitution experiments, or motor/ATPase measurements. This is the principal limitation in assigning a precise biochemical function.
The strongest targeted expression evidence comes from the murine PLRLC literature. PLRLC transcripts were enriched in pre-B-stage lines, with little or no expression in examined pre-T, mature-T, macrophage, fibroblast, and other non-pre-B lines. Adult-bone-marrow-derived pre-B transformants commonly expressed 0.8- and 1.4-kb transcripts, whereas fetal-liver-derived counterparts generally did not. Distinct transcript classes arose from one locus through alternative promoter use and/or RNA processing. (oltz1992anovelregulatory pages 2-3)
IL-7 withdrawal from IL-7-maintained lymphoid bone-marrow cultures caused progressive loss of PLRLC mRNA, while continued IL-7 maintained expression. This establishes cytokine-responsive transcriptional regulation and links the locus to an adult bone-marrow pre-B developmental state. It does not establish that MYL10 transduces IL-7 receptor signaling, nor that it is required for B-cell differentiation. (oltz1992anovelregulatory pages 5-7)
Some unusual PLRLC transcripts contained novel N-terminal, non-myosin sequence joined to MLC-2-related exons, whereas the D transcript resembled conventional RLCs and was the only class detected in skeletal muscle. This transcript complexity makes isoform-resolved human protein studies particularly important. (oltz1992anovelregulatory pages 5-7)
A 2021 genome-wide neural-repair study provides the clearest perturbational phenotype for the mouse ortholog. Investigators delivered an Myl10-targeting sgRNA by AAV to retinal ganglion cells in Cas9-expressing mice, performed optic-nerve crush, and assessed CTB-labeled axons 17 days later. Myl10 loss was among the strongest regeneration-promoting hits, with an effect comparable to Pten; in a complementary neuronal assay, growth exceeded the 500-µm measurement range. AAV2 infected approximately 50% of RGCs, and about 90% of infected cells were RGCs, supporting a largely RGC-autonomous interpretation. (lindborg2021opticnerveregeneration pages 5-7, lindborg2021opticnerveregeneration pages 4-5)
Myl10 editing produced only a trend toward improved RGC survival, while regeneration normalized to surviving cells remained at least as strong as the Pten result. The authors proposed altered actomyosin behavior in growth cones, but did not establish MYL10 localization, its myosin partner, or a molecular mechanism. Sample sizes were approximately 3–10 nerves per gene, and sgRNA efficiency and possible nonautonomous effects remain caveats. (lindborg2021opticnerveregeneration pages 5-7, lindborg2021opticnerveregeneration pages 4-5, lindborg2021opticnerveregeneration pages 12-14)
No high-confidence MYL10-specific localization experiment was identified. Given its RLC fold, a cytoplasmic association with actomyosin structures is plausible. Depending on cell context, that could include contractile filaments, cortical actomyosin, or neuronal growth cones, but these locations should not be recorded as experimentally proven for human Q9BUA6. The protein is not supported as secreted, membrane-spanning, nuclear, or organellar by the evidence reviewed here.
A cautious pathway representation is:
In the peer-reviewed 2024 NPJ Microgravity study, engineered human skeletal-muscle myobundles from young-athletic and old-sedentary donors spent 10 days on the International Space Station. MYL10 RNA was significantly reduced in old-sedentary flight samples versus matched ground controls and was also reduced in young-athletic flight samples. The authors interpreted the joint myosin-expression changes as compatible with altered differentiation and fiber-type remodeling. No MYL10-specific fold change or adjusted P value appeared in the retrieved passage. Most importantly, this was RNA-seq association—not evidence of MYL10 protein loss, altered Ca²⁺ handling, impaired contraction, or causal involvement in microgravity atrophy. Publication: September 2024; URL: https://doi.org/10.1038/s41526-023-00322-y. (parafati2024humanskeletalmuscle pages 2-4, parafati2024humanskeletalmuscle pages 7-7)
A 2024 reanalysis of GEO dataset GSE19567 examined K562 human CML cells after 24 hours of 0.5 µM imatinib or 0.05 µM nilotinib. The authors identified 626 commonly upregulated and 268 commonly downregulated genes; MYL10 was classified as an upregulated network hub. The upregulated PPI network contained 150 nodes and 145 edges, and hub status came from STRING/Cytoscape/MCODE/cytoHubba analysis. There was no MYL10-specific perturbation, protein validation, drug-binding assay, rescue, resistance model, animal experiment, or patient validation. MYL10 is therefore an exploratory treatment-response marker, not a demonstrated BCR–ABL pathway component or therapeutic target. Publication: December 2024; URL: https://doi.org/10.1080/15257770.2023.2296021. (hekmatshoar2024identificationofcommon pages 4-8, hekmatshoar2024identificationofcommon pages 1-4)
A 2023 deep-learning lung-cancer workflow selected MYL10 among 12 computationally investigated genes and predicted 524 candidate inhibitors. Its modeling resource contained 11,330 drug–cell-line interactions, 122 drugs, approximately 32,000 genes, and 106 cell lines. These figures describe computational coverage, not verified ligand binding or MYL10 dependence; they should not be interpreted as 524 experimentally validated MYL10 inhibitors. Publication: November 2023; URL: https://doi.org/10.3389/fbinf.2023.1225149. (chebanov2023analgorithmfor pages 5-7)
Open Targets reports literature-derived MYL10 associations with skin disorder (score 0.307), osteoarthritis (0.259), alcohol drinking (0.226), cardiomyopathy (0.211), and basal-cell carcinoma (0.110). These are low-scoring aggregate associations and do not establish Mendelian causation, tissue mechanism, or therapeutic tractability. (OpenTargets Search: -MYL10)
No approved MYL10-specific drug, clinical assay, companion diagnostic, validated biomarker, or clinical trial emerged from the reviewed evidence. Current applications are research-stage:
| Question/claim | Best evidence | Organism/system | Evidence tier | Conclusion | Key limitation |
|---|---|---|---|---|---|
| Identity and protein family | MYL10 is identified among human myosin regulatory light-chain genes; RLC proteins are calmodulin-like EF-hand proteins. This agrees with UniProt Q9BUA6 and the supplied MYLC2PL/PLRLC aliases and EF-hand/Myosin_RLC domains. (heissler2014myosinlightchains pages 4-5) | Human; sequence/domain classification | Family inference | Human MYL10/Q9BUA6 is an RLC-family EF-hand protein, not MYH10, a MYLK kinase, or MYL2/MYL9/MYL12. | Literature does not independently verify every UniProt feature or demonstrate functional Ca²⁺ binding by purified human MYL10. |
| Pre-B-cell expression and IL-7 regulation | PLRLC transcripts were enriched in murine pre-B-cell subsets; IL-7 withdrawal progressively reduced PLRLC mRNA, whereas continued IL-7 maintained it. Multiple transcripts arose from one locus. (oltz1992anovelregulatory pages 5-7, oltz1992anovelregulatory pages 2-3) | Mouse pre-B-cell lines and bone-marrow cultures | Direct | The murine PLRLC/Myl10 lineage is developmentally regulated and IL-7-responsive at the RNA level. | Predominantly murine, transcript-level evidence; it does not prove an equivalent human lymphocyte protein function. |
| Structural/regulatory myosin role | RLC-family proteins bind myosin heavy-chain neck regions and influence holoenzyme structure and mechanochemical regulation; MYL10 belongs to this family. (heissler2014myosinlightchains pages 4-5) | General myosin/RLC biology | Family inference | Human MYL10 is most plausibly a nonenzymatic myosin-associated structural/regulatory light-chain subunit, rather than an enzyme or transporter. | No direct human-MYL10 reconstitution, motor assay, or MYL10-specific heavy-chain-binding experiment was identified. |
| Exact heavy-chain partner, phosphorylation, Ca²⁺ affinity, and localization | Available MYL10-specific studies do not establish these properties; EF hands in RLC proteins may be degenerate and need not bind Ca²⁺ effectively. (oltz1992anovelregulatory pages 5-7, heissler2014myosinlightchains pages 4-5) | Human MYL10; comparison with RLC family | Family inference | The native myosin partner, phosphorylation sites and kinetics, Ca²⁺-binding affinity, and precise intracellular localization remain unresolved for human MYL10. | General RLC behavior must not be transferred to MYL10 without biochemical or imaging validation. |
| Axon-regeneration phenotype | AAV-sgRNA targeting of Myl10 in Cas9 mice enhanced retinal-ganglion-cell axon regeneration after optic-nerve crush; Myl10 was among the strongest hits, with regeneration comparable to Pten and exceeding the 500-µm in-vitro measurement range. (lindborg2021opticnerveregeneration pages 5-7, lindborg2021opticnerveregeneration pages 4-5, lindborg2021opticnerveregeneration pages 12-14) | Mouse retinal ganglion cells, cortical neurons, and optic-nerve crush | Ortholog perturbation | Mouse Myl10 loss can remove a constraint on injured-axon growth, plausibly through growth-cone actomyosin mechanics. | Mechanism and localization were not demonstrated; survival showed only a trend, sample sizes were limited, and human relevance is unproven. |
| Spaceflight/microgravity response | After 10 days on the ISS, MYL10 RNA was significantly downregulated in old-sedentary human muscle myobundles and was also reduced in young-athletic flight samples versus matched ground controls. (parafati2024humanskeletalmuscle pages 2-4, parafati2024humanskeletalmuscle pages 7-7) | Human skeletal-muscle tissue chips | Association | MYL10 is a candidate marker of microgravity-associated contractile or fiber-type remodeling. | No MYL10-specific fold change was provided in the cited text; RNA association does not establish protein loss, causal function, or altered Ca²⁺ handling. |
| CML drug-response candidate | Reanalysis of GSE19567 found MYL10 among common upregulated network hubs after 24-hour treatment of K562 cells with 0.5 µM imatinib or 0.05 µM nilotinib; 626 genes were commonly upregulated and 268 downregulated. (hekmatshoar2024identificationofcommon pages 4-8, hekmatshoar2024identificationofcommon pages 1-4) | Human K562 chronic-myeloid-leukemia cells; computational microarray/PPI analysis | Association | MYL10 is an exploratory drug-response/network candidate, not an established BCR–ABL-pathway component or drug target. | No MYL10-specific fold change, protein validation, perturbation, binding, rescue, patient, or resistance experiment was reported. |
| Disease associations | Open Targets lists low-scoring links to skin disorder (0.307), osteoarthritis (0.259), alcohol drinking (0.226), cardiomyopathy (0.211), and basal-cell carcinoma (0.110). (OpenTargets Search: -MYL10) | Aggregated human disease–target evidence | Association | Current disease links are hypothesis-generating rather than causal. | Scores are low and literature-derived; they do not demonstrate Mendelian causation, therapeutic tractability, or a MYL10-specific mechanism. |
| Validated clinical applications | Searches identified no approved MYL10 diagnostic, prognostic test, therapeutic agent, clinical trial, or clinically validated biomarker; proposed uses remain computational or preclinical. (OpenTargets Search: -MYL10, lindborg2021opticnerveregeneration pages 5-7, parafati2024humanskeletalmuscle pages 2-4, hekmatshoar2024identificationofcommon pages 4-8) | Clinical/translational landscape | Association | No validated clinical or real-world MYL10 application is currently established. | Absence from retrieved evidence is not proof that no unpublished or newly registered program exists. |
Table: Evidence-tier summary for human MYL10/Q9BUA6, separating direct findings, ortholog perturbations, family-based inference, and associations. It highlights the strongest conclusions and the substantial unresolved biochemical and translational questions.
The literature remains sparse for this specific human protein. The expert-level conclusion should therefore be deliberately narrower than annotations often transferred from MYL9 or MYL12:
Recommended primary annotation: Human MYL10/Q9BUA6 is a poorly characterized EF-hand, myosin-regulatory-light-chain-family protein, probably serving as a nonenzymatic structural/regulatory component of an actomyosin motor complex. Its locus shows developmental and cytokine-responsive regulation in the murine precursor-B lineage; mouse loss-of-function promotes axon regeneration; and human MYL10 transcript abundance responds to microgravity and kinase-inhibitor exposure. The native human myosin complex, biochemical regulatory mechanism, and physiological necessity remain unknown.
The highest-priority experiments are endogenous affinity purification/proximity labeling to identify heavy-chain partners; isoform-resolved long-read RNA sequencing; CRISPR knockout and rescue with Q9BUA6 in human lymphoid, muscle, and neuronal systems; phosphoproteomics followed by kinase/phosphatase assays; purified-protein Ca²⁺/Mg²⁺ binding measurements; and endogenous-tag live-cell imaging. Until those studies are available, specific claims about calcium sensing, MLCK-dependent activation, sarcomere localization, or clinical actionability should be regarded as unproven.
References
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(oltz1992anovelregulatory pages 2-3): E. Oltz, G. Yancopoulos, Maureen A. Morrow, Anton Rolink, Grace M. Lee, Franklin Wong, Kenneth Kaplan, Steve Gillis, F. Melchers, and Frederick W. Alt. A novel regulatory myosin light chain gene distinguishes pre‐b cell subsets and is il‐7 inducible. The EMBO Journal, 11:2759-2767, Jul 1992. URL: https://doi.org/10.1002/j.1460-2075.1992.tb05341.x, doi:10.1002/j.1460-2075.1992.tb05341.x. This article has 61 citations.
(heissler2014myosinlightchains pages 4-5): Sarah M Heissler and James R Sellers. Myosin light chains: teaching old dogs new tricks. Bioarchitecture, 4:169-188, Jun 2014. URL: https://doi.org/10.1080/19490992.2015.1054092, doi:10.1080/19490992.2015.1054092. This article has 190 citations.
(lindborg2021opticnerveregeneration pages 5-7): Jane A. Lindborg, Nicholas M. Tran, Devon M. Chenette, Kristin DeLuca, Yram Foli, Ramakrishnan Kannan, Yuichi Sekine, Xingxing Wang, Marius Wollan, In-Jung Kim, Joshua R. Sanes, and Stephen M. Strittmatter. Optic nerve regeneration screen identifies multiple genes restricting adult neural repair. Cell reports, 34:108777-108777, Mar 2021. URL: https://doi.org/10.1016/j.celrep.2021.108777, doi:10.1016/j.celrep.2021.108777. This article has 71 citations and is from a highest quality peer-reviewed journal.
(lindborg2021opticnerveregeneration pages 4-5): Jane A. Lindborg, Nicholas M. Tran, Devon M. Chenette, Kristin DeLuca, Yram Foli, Ramakrishnan Kannan, Yuichi Sekine, Xingxing Wang, Marius Wollan, In-Jung Kim, Joshua R. Sanes, and Stephen M. Strittmatter. Optic nerve regeneration screen identifies multiple genes restricting adult neural repair. Cell reports, 34:108777-108777, Mar 2021. URL: https://doi.org/10.1016/j.celrep.2021.108777, doi:10.1016/j.celrep.2021.108777. This article has 71 citations and is from a highest quality peer-reviewed journal.
(lindborg2021opticnerveregeneration pages 12-14): Jane A. Lindborg, Nicholas M. Tran, Devon M. Chenette, Kristin DeLuca, Yram Foli, Ramakrishnan Kannan, Yuichi Sekine, Xingxing Wang, Marius Wollan, In-Jung Kim, Joshua R. Sanes, and Stephen M. Strittmatter. Optic nerve regeneration screen identifies multiple genes restricting adult neural repair. Cell reports, 34:108777-108777, Mar 2021. URL: https://doi.org/10.1016/j.celrep.2021.108777, doi:10.1016/j.celrep.2021.108777. This article has 71 citations and is from a highest quality peer-reviewed journal.
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(OpenTargets Search: -MYL10): Open Targets Query (-MYL10, 5 results). Buniello, A. et al. (2025). Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery. Nucleic Acids Research.