TMOD3 Human

What is TMOD3 and what are its primary functions in human cells?

TMOD3 (Tropomodulin 3) is a ubiquitously expressed member of the tropomodulin family of proteins that caps the pointed ends of actin filaments. Its primary functions include:

• Blocking elongation and depolymerization of actin filaments at their pointed ends

• Contributing to the formation of short actin protofilaments that define membrane skeleton geometry

• Enabling cadherin binding involved in cell-cell adhesion processes

• Participating in actin cytoskeleton organization and regulation

• Acting in pathways related to Rho GTPase signaling

TMOD3 is particularly notable as the only Tmod isoform identified in the human platelet proteome, with approximately 11,900 copies per platelet, though it is considerably less abundant than other actin-regulating proteins like cofilin . Understanding TMOD3's role in actin regulation provides fundamental insights into cytoskeletal dynamics that influence multiple cellular processes.

How does TMOD3 differ from other tropomodulin family members?

TMOD3 differs from other tropomodulin family members (TMOD1, TMOD2, and TMOD4) in several important ways:

• Expression pattern: While TMOD1, TMOD2, and TMOD4 show tissue-specific expression, TMOD3 is ubiquitously expressed across tissues , making it a more versatile research target for studying general cellular functions.

• Evolutionary relationship: TMOD2 and TMOD3 are the most closely related family members, with their genes located in close proximity on human chromosome 15q21.1-q21.2 (chromosome 9 in mice) . This suggests a relatively recent gene duplication event.

• Developmental significance: Unlike TMOD1 knockout mice that survive to adulthood with erythrocyte defects, TMOD3 knockout mice are embryonic lethal by E18.5, suggesting more critical developmental functions .

• Morphological impact: In neuronal studies, TMOD3 has shown only minor influence on morphology compared to TMOD1 and TMOD2, which significantly regulate dendritic arbor and spine morphology .

• Gene structure: The TMOD3 gene has several developmentally regulated transcripts ranging from ~1 kb to ~9.5 kb that remain largely uncharacterized , suggesting additional complexity in its regulation.

These differences highlight the specialized roles of each tropomodulin family member in tissue-specific cytoskeletal organization and function.

What are the key structural domains of TMOD3 protein and how do they relate to its function?

TMOD3, like other tropomodulins, contains two major functional domains with distinct structural properties that contribute to its actin-regulating capabilities:

The functional integration of these domains enables TMOD3 to effectively cap actin filaments at their pointed ends. Molecular dynamics simulations have characterized structural changes in the C-terminal helix of the LRR domain when mutations are introduced, revealing how these alterations affect binding to actin monomers . Both domains are required for proper function, as demonstrated by studies showing that disruption of either actin-binding site compromises the ability of tropomodulins to regulate cellular morphology .

What experimental approaches are most effective for studying TMOD3's interaction with the actin cytoskeleton?

Studying TMOD3's interactions with the actin cytoskeleton requires multi-faceted experimental approaches:

• Proximity Ligation Assays (PLAs):

  • Highly effective for detecting and quantifying TMOD3's in situ interactions with binding partners like tropomyosins Tpm3.1 and Tpm3.2

  • Provides spatial information about interaction sites within cells

  • Can confirm how mutations in actin-binding domains affect protein-protein interactions

• Molecular Dynamics Simulations (MDS):

  • Critical for characterizing structural changes caused by mutations in TMOD3's domains

  • Helps predict how alterations affect binding to actin monomers

  • Provides atomic-level insights into functional mechanisms

• Overexpression of Mutated Forms:

  • Systematic mutation of actin-binding sites followed by overexpression in relevant cell types

  • Analysis of resulting morphological changes provides functional insights

  • Can be combined with live-cell imaging to track dynamic effects

• Biochemical Assays:

  • In vitro actin polymerization/depolymerization assays to directly measure TMOD3's capping activity

  • Sedimentation assays to analyze TMOD3's effects on actin filament stability

  • Cross-linking experiments to identify potential TMOD3 complexes or dimerization

• Biophysical Characterization Methods:

  • Synchrotron small-angle X-ray scattering to determine TMOD3's molecular dimensions and shape

  • Analysis of Stokes radius and sedimentation coefficient to understand hydrodynamic properties

These complementary approaches provide comprehensive insights into how TMOD3 regulates actin dynamics in different cellular contexts.

How does TMOD3 overexpression contribute to platinum resistance in ovarian cancer, and what are the implications for cancer research?

TMOD3 overexpression has emerged as a significant marker for platinum resistance in ovarian cancer with important research implications:

These findings suggest several research avenues: development of TMOD3 inhibitors as platinum-sensitizing agents, exploration of TMOD3's role in modulating tumor immune responses, and investigation of the TMOD3-associated gene network as a therapeutic target in resistant disease.

What role does TMOD3 play in neuronal development and function, and how does it compare to other tropomodulin isoforms?

TMOD3's role in neuronal development differs significantly from other tropomodulin isoforms:

• Relative Impact on Neuronal Morphology:

  • Unlike TMOD1 and TMOD2, which strongly regulate dendritic arbor and spine morphology, TMOD3 exerts only minor influences on neuronal morphology

  • This suggests specialized division of labor among tropomodulin family members in the nervous system

• Actin-Binding Requirements:

  • Studies of TMOD1 and TMOD2 in hippocampal neurons show both require their two actin-binding sites to properly regulate dendritic morphology and spine shape

  • These findings suggest TMOD3 may function through similar mechanisms but with different efficacy or in different neuronal compartments

• Tropomyosin Interactions:

  • TMOD3 likely interacts with specific tropomyosin isoforms in neurons, including Tpm3.1 and Tpm3.2

  • These interactions influence actin stability in neuronal structures

  • The specific tropomyosin partners may partly explain functional differences between TMOD isoforms

• Expression Patterns:

  • TMOD3 is expressed in various brain regions including the hippocampal formation, amygdala, basal ganglia, midbrain, spinal cord, cerebral cortex, cerebellum, and hypothalamus

  • The widespread expression suggests general housekeeping functions in neurons compared to more specialized roles for other isoforms

Understanding these differences provides insight into how neurons utilize specific cytoskeletal regulators to achieve precise control over morphology and function during development and in response to stimuli.

What are the most reliable methods for detecting and quantifying TMOD3 expression in different human tissues?

Reliable detection and quantification of TMOD3 in human tissues requires consideration of several complementary approaches:

• Immunohistochemistry (IHC)/Immunofluorescence (IF):

  • The Human Protein Atlas provides validated antibodies and standardized protocols for TMOD3 detection across tissues

  • Critical considerations include fixation methods that preserve cytoskeletal architecture

  • Co-staining with actin markers enhances localization accuracy

  • Quantification should include both intensity and distribution patterns

• Western Blotting:

  • Effective for quantifying total TMOD3 protein levels

  • Requires careful sample preparation to preserve intact protein

  • Comparison with housekeeping genes must account for tissue-specific variation

  • Can detect the ~40 kDa TMOD3 protein across various tissue extracts

• Quantitative RT-PCR:

  • Useful for analyzing transcript levels of the multiple TMOD3 transcripts (ranging from ~1 kb to ~9.5 kb)

  • Requires careful primer design to distinguish TMOD3 from other tropomodulin family members

  • Should target conserved regions across the multiple transcripts

• RNA-Seq/Transcriptomics:

  • Provides comprehensive view of TMOD3 expression across tissues

  • Allows detection of alternative transcripts and splicing variants

  • Can identify co-expressed genes for pathway analysis

  • Resources like GeneCards, NCBI Gene, and Ensembl provide reference expression data

• Proteomics:

  • Mass spectrometry-based approaches can quantify TMOD3 protein levels

  • The Clinical Proteomic Tumor Analysis Consortium (CPTAC) database offers valuable reference data for cancer tissues

  • Label-free quantification methods are particularly valuable for comparative studies

When implementing these methods, researchers should consider tissue-specific expression levels, with TMOD3 showing ubiquitous expression but varying levels across tissues .

What knockout or knockdown approaches have proven most effective for studying TMOD3 function in experimental models?

Several genetic manipulation approaches have been employed to study TMOD3 function, each with specific advantages and limitations:

• Germline Knockout Models:

  • Complete TMOD3 knockout in mice is embryonic lethal by E18.5, limiting adult studies

  • Heterozygous models (TMOD3+/-) provide viable alternatives for studying partial loss of function

  • Embryonic lethality indicates essential developmental roles, with embryos showing hemorrhaging at E14.5

  • Platelet defects (fewer and larger platelets) observed in knockout embryos highlight TMOD3's role in megakaryocyte development

• Conditional Knockout Approaches:

  • Tissue-specific Cre-loxP systems overcome embryonic lethality

  • Temporal control using inducible systems allows study of TMOD3 function at specific developmental stages

  • Particular value in studying tissue-specific functions in hematopoietic and neuronal systems

• RNA Interference (RNAi):

  • siRNA and shRNA approaches provide transient or stable knockdown options

  • Allows titration of knockdown levels to study dose-dependent effects

  • Particularly useful in cell culture models of actin dynamics

  • Can reveal acute versus chronic adaptation to TMOD3 reduction

• CRISPR/Cas9 Gene Editing:

  • Enables precise modification of TMOD3 domains (LRR-Cap or TM-Cap domains)

  • Can be used to create specific mutations that mimic those used in structural studies

  • Allows creation of point mutations that disrupt actin binding without eliminating the entire protein

• Overexpression of Dominant-Negative Mutants:

  • Expression of TMOD3 with mutations in actin-binding sites can disrupt function of endogenous protein

  • Permits study of specific functional domains without complete protein loss

  • Has been effectively used to study tropomodulin effects on dendritic morphology

When designing TMOD3 loss-of-function studies, researchers should consider compensatory upregulation of other tropomodulin family members, particularly TMOD2, which shares the highest sequence similarity with TMOD3 .

How can researchers effectively investigate TMOD3's interactions with tropomyosins and their combined effect on actin dynamics?

Investigating TMOD3's interactions with tropomyosins requires specialized techniques to capture these dynamic molecular relationships:

• Co-Immunoprecipitation (Co-IP) and Pull-Down Assays:

  • Effective for identifying direct binding between TMOD3 and specific tropomyosin isoforms

  • Should be performed under native conditions to preserve physiological interactions

  • Can be combined with mass spectrometry to identify novel interaction partners

  • Quantitative analysis can reveal binding affinities between TMOD3 and different tropomyosin isoforms

• Proximity Ligation Assays (PLAs):

  • Particularly valuable for detecting in situ interactions between TMOD3 and tropomyosins

  • Provides spatial information about where in the cell these interactions occur

  • Can quantify how mutations affect TMOD3-tropomyosin binding

  • Especially effective for studying interactions with Tpm3.1 and Tpm3.2 in neuronal contexts

• Fluorescence Resonance Energy Transfer (FRET):

  • Allows real-time visualization of TMOD3-tropomyosin interactions in living cells

  • Can detect conformational changes upon binding

  • Particularly useful for studying how these interactions change during dynamic cellular processes

• In Vitro Reconstitution Assays:

  • Purified components can be used to study direct effects on actin polymerization kinetics

  • Allows precise control of protein concentrations and conditions

  • Can determine how TMOD3 and tropomyosins synergistically regulate actin filament pointed ends

  • Total internal reflection fluorescence (TIRF) microscopy can visualize these effects at the single-filament level

• Structural Biology Approaches:

  • X-ray crystallography and cryo-electron microscopy can reveal atomic details of interactions

  • Molecular dynamics simulations help predict how mutations affect these interactions

  • Small-angle X-ray scattering has been effective in characterizing TMOD structure and may reveal TMOD3-tropomyosin complexes

These approaches are particularly important because the Tmod/tropomyosin complex contributes to the formation of short actin protofilaments that define membrane skeleton geometry , with implications for cellular architecture and function.

What disease associations have been established for TMOD3, and what are the molecular mechanisms involved?

TMOD3 has been implicated in several diseases through various molecular mechanisms:

Understanding these disease associations provides valuable research directions for therapeutic development, with TMOD3 representing a potential biomarker or target in conditions like platinum-resistant ovarian cancer.

How does TMOD3 contribute to platelet biogenesis and what are the implications for hematological research?

TMOD3's role in platelet biogenesis has significant implications for hematological research:

• Megakaryocyte Development and Platelet Formation:

  • TMOD3 knockout mice (TMOD3-/-) exhibit hemorrhaging at E14.5 with fewer but larger platelets

  • This phenotype directly implicates TMOD3 in regulating platelet size and number during development

  • TMOD3 is the only tropomodulin isoform identified in the human platelet proteome, with approximately 11,900 copies per platelet

• Cytoskeletal Regulation During Thrombopoiesis:

  • TMOD3's actin-capping function likely regulates the extensive cytoskeletal remodeling required during platelet production

  • Proper actin dynamics are essential for proplatelet extension from megakaryocytes and platelet shedding

  • TMOD3 may work with platelet-specific tropomyosins to control these processes

• Megakaryocyte Maturation:

  • TMOD3-/- fetal livers show moderately increased megakaryocyte numbers with only a slight increase in the 8N population

  • This suggests TMOD3 may not significantly affect megakaryocyte differentiation but rather subsequent platelet formation

  • The specific stage of platelet biogenesis affected appears to be after megakaryocyte formation

• Research Implications:

  • TMOD3 represents a potential target for modulating platelet production in thrombocytopenic disorders

  • Understanding TMOD3's role provides insights into fundamental mechanisms of thrombopoiesis

  • Conditional knockout models could enable studies of TMOD3 function in adult megakaryopoiesis

  • Study of TMOD3 interactions with other cytoskeletal regulators in megakaryocytes could reveal novel therapeutic targets

These findings highlight TMOD3 as an important regulator of terminal stages of platelet production, with potential therapeutic implications for bleeding disorders and conditions requiring platelet transfusions.

What are the most promising unexplored aspects of TMOD3 biology for future research?

Several unexplored aspects of TMOD3 biology offer promising avenues for future research:

• Transcriptional and Post-Transcriptional Regulation:

  • The TMOD3 gene has several developmentally regulated transcripts ranging from ~1 kb to ~9.5 kb that remain largely uncharacterized

  • Understanding the functional significance of these different transcripts could reveal tissue-specific regulatory mechanisms

  • Investigation of microRNA regulation of TMOD3, particularly in disease contexts like cancer

• Structural Biology of TMOD3 Complexes:

  • High-resolution structures of TMOD3 in complex with actin and/or tropomyosin are lacking

  • Understanding these structures could inform design of specific inhibitors or modulators

  • Comparative structural analysis with other tropomodulin isoforms could explain functional differences

• Role in Immune Cell Function:

  • TMOD3 expression correlates with immune infiltration in cancer , suggesting unexplored functions in immune cells

  • Investigation of TMOD3's role in immune cell migration, activation, and effector functions

  • Potential impact on immunotherapy response through cytoskeletal regulation

• Therapeutic Targeting Approaches:

  • Development of small molecule inhibitors specific to TMOD3's actin-binding or tropomyosin-binding domains

  • Exploration of TMOD3 as a sensitizing target for chemotherapy resistance in cancer

  • Evaluation of TMOD3 modulation for hematological disorders affecting platelet production

• Compensatory Mechanisms Among Tropomodulins:

  • Investigation of how other tropomodulin family members compensate for TMOD3 loss in different tissues

  • Understanding the redundancy and specificity in the tropomodulin family

  • Identification of contexts where combined targeting of multiple tropomodulins might be necessary

These research directions could significantly advance our understanding of TMOD3 biology and reveal new therapeutic opportunities across multiple disease contexts.

What emerging technologies and methodologies are likely to advance TMOD3 research in the next decade?

Emerging technologies poised to transform TMOD3 research include:

• Cryo-Electron Microscopy (Cryo-EM):

  • Will enable visualization of TMOD3-actin-tropomyosin complexes at near-atomic resolution

  • Can capture different conformational states during actin capping

  • May reveal previously uncharacterized protein-protein interactions

• Single-Cell Multi-Omics:

  • Integration of transcriptomics, proteomics, and functional genomics at single-cell level

  • Will reveal cell-type specific TMOD3 expression patterns and functions

  • Particularly valuable for understanding TMOD3's role in heterogeneous tissues and tumors

• Live-Cell Super-Resolution Microscopy:

  • Techniques like PALM, STORM, and lattice light-sheet microscopy

  • Will allow real-time visualization of TMOD3's interaction with actin filaments in living cells

  • Can track dynamic changes during cellular processes like migration or division

• Proteomics-Based Interactome Mapping:

  • BioID, APEX proximity labeling, or mass spectrometry-based approaches

  • Will identify comprehensive TMOD3 protein interaction networks

  • May reveal previously unknown binding partners beyond actin and tropomyosin

• CRISPR-Based Genetic Screening:

  • Genome-wide or targeted screens to identify genetic modifiers of TMOD3 function

  • Can uncover synthetic lethal interactions in cancer contexts

  • Will help place TMOD3 in broader cellular signaling networks

• Organoid and Tissue Engineering Technologies:

  • Will enable study of TMOD3 in physiologically relevant 3D models

  • Particularly valuable for developmental studies that are challenging in vivo

  • Can model disease states and test therapeutic approaches

• Machine Learning Approaches:

  • Analysis of large-scale cytoskeletal imaging data

  • Prediction of TMOD3 binding partners and functional interactions

  • Integration of multi-omics data to build predictive models of TMOD3 function

These technologies will collectively drive significant advances in understanding TMOD3's structural properties, cellular functions, and disease relevance, enabling more targeted therapeutic approaches.

What practical advice would you give to researchers beginning TMOD3-focused projects?

For researchers initiating TMOD3-focused projects, the following practical considerations are essential:

• Choose Appropriate Model Systems:

  • Consider that complete TMOD3 knockout is embryonic lethal in mice

  • Cell lines with high endogenous TMOD3 expression provide good models for loss-of-function studies

  • Neuronal or hematopoietic models are particularly relevant given TMOD3's functional roles in these systems

  • Cancer cell lines with platinum resistance mechanisms may be valuable for studying TMOD3's role in drug resistance

• Antibody and Tool Validation:

  • Rigorously validate TMOD3 antibodies to ensure specificity against other tropomodulin family members

  • The UniProtKB/Swiss-Prot identifier Q9NYL9 can help identify validated reagents

  • Consider using epitope-tagged constructs for studies where antibody specificity is challenging

  • Validate siRNA or shRNA tools to confirm specific TMOD3 knockdown without off-target effects

• Experimental Design Considerations:

  • Always examine potential compensatory upregulation of other tropomodulin isoforms

  • Include appropriate cytoskeletal markers to contextualize TMOD3 findings

  • Design experiments that distinguish between acute and chronic effects of TMOD3 manipulation

  • Consider the potential impact of cell density and matrix interactions on TMOD3-dependent phenotypes

• Analytical Approaches:

  • Implement quantitative image analysis for morphological studies

  • Use multiple complementary techniques to confirm protein-protein interactions

  • Consider both transcript and protein-level analyses given the complexity of TMOD3 regulation

  • Integrate findings with existing datasets using GeneCards, TCGA, CPTAC, and other databases

• Collaboration Opportunities:

  • Given TMOD3's diverse functions, collaborative approaches spanning cytoskeletal biology, cancer research, neuroscience, and hematology can be highly productive

  • Consider partnerships with structural biologists for detailed molecular insights

  • Bioinformatics collaborations can help integrate TMOD3 into broader pathway analyses

These practical considerations will help researchers design robust studies that meaningfully advance understanding of TMOD3 biology.

How should researchers interpret conflicting data regarding TMOD3 function across different experimental systems?

When encountering conflicting data about TMOD3 function, researchers should consider these analytical approaches:

• Contextual Differences Analysis:

  • Systematically compare the cellular contexts of conflicting studies (cell types, tissues, developmental stages)

  • TMOD3 functions may differ significantly between tissues due to varied expression of interaction partners

  • Different experimental models (in vitro, cell culture, animal models) may reveal context-dependent functions

• Methodological Variation Assessment:

  • Evaluate differences in techniques used (genetic manipulation vs. pharmacological approaches)

  • Consider the duration of TMOD3 manipulation (acute vs. chronic), as compensatory mechanisms may emerge over time

  • Assess the specificity and efficiency of tools used (antibodies, siRNAs, genetic constructs)

• Interaction Partner Landscape:

  • Analyze differences in tropomyosin isoform expression across experimental systems

  • TMOD3 function depends critically on its interaction with specific tropomyosins

  • Expression levels of other actin-binding proteins may influence TMOD3's relative importance

• Quantitative Considerations:

  • TMOD3 concentration effects may be non-linear, with different outcomes at varying expression levels

  • In platelets, TMOD3 is present at approximately 11,900 copies per cell , but this may vary significantly across cell types

  • The ratio of TMOD3 to actin and other cytoskeletal components likely influences function

• Integration Strategies:

  • Develop working models that accommodate seemingly contradictory observations

  • Consider that different aspects of TMOD3 function may be revealed by different experimental approaches

  • Use meta-analysis approaches when sufficient data is available across multiple studies

When reporting research findings, explicitly discuss how your results relate to apparent contradictions in the literature, considering these contextual factors to advance a more nuanced understanding of TMOD3 biology.

What are common technical challenges in TMOD3 research and how can they be addressed?

Researchers frequently encounter specific technical challenges when studying TMOD3:

• Antibody Cross-Reactivity Issues:

  • Challenge: TMOD3 antibodies may cross-react with other tropomodulin family members due to sequence similarity, particularly with TMOD2 .

  • Solution: Validate antibodies using TMOD3 knockout or knockdown samples; consider using tagged TMOD3 constructs; perform peptide competition assays to confirm specificity.

• Preserving Cytoskeletal Architecture:

  • Challenge: Standard fixation methods may disrupt the native cytoskeletal architecture, altering TMOD3 localization.

  • Solution: Optimize fixation protocols (e.g., pre-extraction methods that preserve cytoskeletal elements); compare multiple fixation approaches; use live-cell imaging when possible.

• Functional Redundancy Among Tropomodulins:

  • Challenge: Compensatory upregulation of other tropomodulins may mask TMOD3-specific phenotypes.

  • Solution: Use acute knockdown or rapid protein degradation approaches; simultaneously monitor expression of all tropomodulin family members; consider combined knockdown strategies.

• Recombinant Protein Solubility:

  • Challenge: Producing soluble, correctly folded recombinant TMOD3 for biochemical studies.

  • Solution: Optimize expression conditions (temperature, induction time); use solubility tags; consider expressing functional domains separately; employ eukaryotic expression systems.

• Quantifying Actin Dynamics Changes:

  • Challenge: Accurately measuring subtle changes in actin dynamics upon TMOD3 manipulation.

  • Solution: Implement fluorescence recovery after photobleaching (FRAP); use fluorescent actin probes; employ single-filament TIRF microscopy; consider computational modeling to interpret results.

• Translating In Vitro Findings to Cellular Context:

  • Challenge: Determining whether in vitro biochemical results reflect TMOD3's cellular functions.

  • Solution: Design cellular experiments that directly test biochemical observations; use structure-guided mutations to link molecular and cellular phenotypes; employ proximity labeling to identify relevant in vivo binding partners.

What bioinformatic resources and tools are most valuable for TMOD3 research?

Several specialized bioinformatic resources and tools are particularly valuable for TMOD3 research:

• Sequence and Structure Databases:

  • UniProtKB/Swiss-Prot (Q9NYL9): Provides curated TMOD3 protein information, including functional domains and post-translational modifications

  • RCSB Protein Data Bank: Contains structural information for tropomodulin domains that can inform TMOD3 research

  • AlphaFold DB: Offers predicted TMOD3 structures that can guide experimental design

• Expression and Function Databases:

  • Human Protein Atlas: Displays TMOD3 expression patterns across human tissues

  • GeneCards: Integrates diverse TMOD3 information, including disease associations and pathway involvement

  • NCBI Gene (29766): Provides comprehensive gene information and links to related resources

  • Open Targets Platform (ENSG00000138594): Maps TMOD3 to diseases and potential therapeutic relevance

• Cancer and Disease Resources:

  • The Cancer Genome Atlas (TCGA): Contains TMOD3 expression data across cancer types

  • Clinical Proteomic Tumor Analysis Consortium (CPTAC): Offers proteomic data including TMOD3 levels in tumors

  • Gene Expression Omnibus (GEO): Houses numerous datasets containing TMOD3 expression in various experimental contexts

• Protein Interaction Tools:

  • STRING: Maps protein-protein interactions and functional associations for TMOD3

  • BioGRID: Catalogues TMOD3 physical and genetic interactions

  • LinkedOmics: Enables exploration of TMOD3 co-expression networks in cancer contexts

• Immune Analysis Resources:

  • Tumor Immune Estimation Resource (TIMER): Evaluates relationships between TMOD3 expression and immune infiltration

  • TISIDB (integrated repository portal for tumor-immune system interactions): Analyzes TMOD3's relationship with tumor immunity

• Prediction Tools:

  • TargetScan: Predicts microRNAs targeting TMOD3, valuable for understanding post-transcriptional regulation

  • NetPhos: Identifies potential phosphorylation sites that may regulate TMOD3 function

Researchers should integrate data from these diverse resources to develop comprehensive models of TMOD3 function and regulation in their specific research context.