TCEAL7 Human

What is the basic structure and function of TCEAL7 in human cells?

TCEAL7 is a member of the transcription elongation factor A (SII)-like gene family. It functions as a nuclear protein involved in transcriptional regulation. Structurally, TCEAL7 contains conserved E-box motifs within its promoter region that are essential for its activity and regulation . As a transcriptional modulator, TCEAL7 has been shown to repress cellular transformation by negatively regulating key oncogenic pathways, including Myc and NF-κB signaling .

For researchers studying TCEAL7 structure-function relationships, a combination of bioinformatic analysis, protein modeling, and deletion/mutation constructs is recommended to identify functional domains. Experimental approaches should include EMSA (electrophoretic mobility-shift assays) and ChIP (chromatin immunoprecipitation) assays to determine DNA-binding capabilities and genomic targets.

How is TCEAL7 expression regulated in normal human tissues?

TCEAL7 expression is regulated through multiple mechanisms. In skeletal muscle, myogenic regulatory factors (MRFs) directly transactivate TCEAL7 expression by binding to conserved E-box motifs in its promoter region . This regulation has been demonstrated through transgenic reporter assays and chromatin immunoprecipitation experiments.

Epigenetic regulation also plays a crucial role, as TCEAL7 is frequently inactivated by methylation in cancer cells . For researchers investigating TCEAL7 regulation, methodological approaches should include:

• Promoter analysis using reporter assays with wild-type and mutated E-box motifs

• ChIP-seq to identify transcription factors binding to the TCEAL7 promoter

• DNA methylation analysis through bisulfite sequencing

• Analysis of histone modifications using ChIP-qPCR

What experimental systems are most suitable for studying TCEAL7 function?

Based on current research, the following experimental systems are recommended for TCEAL7 studies:

For optimal results, researchers should consider combining multiple models to validate findings across different experimental systems .

How can researchers accurately measure TCEAL7 expression levels in tissue samples?

For reliable quantification of TCEAL7 expression, researchers should employ multiple complementary techniques:

RNA-level analysis:

• RT-qPCR using validated primers spanning exon-exon junctions

• RNA-seq for comprehensive transcriptomic analysis

• In situ hybridization for spatial expression patterns

Protein-level analysis:

• Western blotting with validated antibodies

• Immunohistochemistry for tissue localization

• Immunofluorescence for subcellular localization

For optimal results, researchers should normalize TCEAL7 expression to multiple housekeeping genes or proteins when performing quantitative analyses. This approach has been successfully used in studies examining TCEAL7 expression in gastric cancer tissues compared to matched adjacent non-tumor tissues .

What are the key transcription factors that regulate TCEAL7 expression?

Based on current research, several transcription factors regulate TCEAL7:

• Myogenic Regulatory Factors (MRFs): MyoD, myogenin, Myf5, and MRF4 have been shown to directly bind to conserved E-box motifs in the TCEAL7 promoter and transactivate its expression .

• E-box binding proteins: The 0.7 kb upstream fragment of the TCEAL7 gene contains evolutionarily conserved E-box motifs that are essential for promoter activity .

To identify additional transcription factors, researchers should consider:

• Computational prediction using transcription factor binding site databases

• Yeast one-hybrid screening

• ChIP-seq analysis of candidate transcription factors

• CRISPR-based transcription factor screening

How does TCEAL7 expression change during cellular differentiation?

TCEAL7 expression is dynamically regulated during cellular differentiation, particularly in the skeletal muscle lineage. During muscle differentiation:

• TCEAL7 expression increases as cells exit the cell cycle and commit to differentiation

• Overexpression of TCEAL7 in C2C12 myoblasts decreases cellular proliferation and enhances differentiation

• TCEAL7 upregulates p27 expression, a key cell cycle inhibitor that promotes myogenic differentiation

To study TCEAL7's role in differentiation, researchers should:

• Monitor TCEAL7 expression throughout differentiation time courses

• Perform gain- and loss-of-function studies using overexpression and knockdown approaches

• Analyze cell cycle dynamics and differentiation markers

• Investigate downstream effectors through transcriptomic and proteomic analyses

What is the relationship between TCEAL7 expression and cancer progression?

TCEAL7 appears to function as a tumor suppressor in multiple cancer types:

• Ovarian cancer: TCEAL7 is inactivated by methylation in ovarian cancer cells .

• Gastric cancer:

  • TCEAL7 expression is significantly decreased in 43.3% of gastric adenocarcinoma cases

  • Low TCEAL7 expression correlates with larger tumor size, higher histological grade, and worse nodal status

  • Reduced TCEAL7 expression is associated with poor prognosis in gastric cancer patients

  • Multivariate analysis identifies TCEAL7 expression as an independent risk factor in gastric cancer prognosis

For researchers investigating TCEAL7 in cancer, methodological approaches should include:

• Analysis of TCEAL7 expression in tumor tissue microarrays

• Correlation of TCEAL7 levels with clinicopathological features

• Survival analysis based on TCEAL7 expression

• Functional studies in cancer cell lines to determine mechanisms of tumor suppression

How can researchers effectively restore TCEAL7 function in disease models?

Several approaches can be considered for restoring TCEAL7 function in disease models:

• Gene therapy approaches:

  • Viral vectors (adenovirus, lentivirus) expressing TCEAL7

  • Non-viral delivery systems (liposomes, nanoparticles)

• Epigenetic modulation:

  • DNA methyltransferase inhibitors to reverse methylation-based silencing

  • Histone deacetylase inhibitors to modify chromatin structure

• Transcriptional activation:

  • CRISPR-based activation systems targeting the TCEAL7 promoter

  • Small molecules that enhance MRF-mediated activation

Researchers should validate restoration of TCEAL7 expression through qPCR and western blotting, followed by functional assays to confirm phenotypic rescue in disease models.

What are the contradictions in published data regarding TCEAL7's role in different cancer types?

While limited data is available from the search results, potential contradictions may arise in TCEAL7 research regarding:

• Tissue-specific effects: TCEAL7 may have different functions in different tissue contexts, requiring tissue-specific analysis rather than generalizing across cancer types.

• Mechanistic contradictions: The pathways through which TCEAL7 exerts its tumor suppressor function may vary between cancer types. In some contexts, it may work primarily through Myc inhibition, while in others, NF-κB modulation may be more important .

• Prognostic relevance: While decreased TCEAL7 expression correlates with poor prognosis in gastric cancer , this relationship may not be universal across all cancer types.

To resolve these contradictions, researchers should:

• Perform meta-analyses of TCEAL7 expression across multiple cancer datasets

• Design comparative studies across different cancer types using identical methodologies

• Investigate tissue-specific interactors that may modify TCEAL7 function

What are the most reliable antibodies and reagents for studying TCEAL7?

While specific antibody recommendations are not provided in the search results, researchers should consider the following when selecting reagents for TCEAL7 studies:

When publishing TCEAL7 research, detailed methodology sections should include catalog numbers, validation data, and specific protocols to ensure reproducibility.

How can researchers differentiate between TCEAL7 and other TCEAL family members in functional studies?

The TCEAL gene family contains several members with potential functional overlap. To specifically study TCEAL7:

• Expression analysis:

  • Design primers that target unique regions of TCEAL7

  • Compare expression patterns of all TCEAL family members as done in gastric cancer cell lines

• Specific knockdown:

  • Design siRNAs targeting unique 3'UTR regions

  • Validate specificity by measuring expression of all family members

• Rescue experiments:

  • Perform rescue experiments with TCEAL7 constructs resistant to siRNA

  • Create chimeric proteins to identify functional domains specific to TCEAL7

• Evolutionary analysis:

  • Analyze conservation patterns to identify TCEAL7-specific motifs

  • Use comparative genomics to understand functional divergence

What high-throughput approaches are most informative for investigating TCEAL7 function?

For comprehensive characterization of TCEAL7 function, researchers should consider these high-throughput approaches:

• Transcriptomic analyses:

  • RNA-seq following TCEAL7 overexpression or knockdown

  • Single-cell RNA-seq to identify cell-type specific responses

  • Temporal transcriptomics during differentiation or disease progression

• Proteomic approaches:

  • Mass spectrometry to identify TCEAL7 interacting partners

  • Phosphoproteomics to identify signaling pathways affected by TCEAL7

  • RIME (Rapid Immunoprecipitation Mass spectrometry of Endogenous proteins) for chromatin-associated interactions

• Epigenomic analyses:

  • ChIP-seq to identify genomic binding sites

  • ATAC-seq to assess chromatin accessibility changes

  • CUT&RUN for high-resolution binding profiles

• Functional genomics:

  • CRISPR screens to identify synthetic lethal interactions

  • Genetic dependency mapping in cancer cell lines

These approaches should be integrated through computational analysis to develop comprehensive models of TCEAL7 function in normal and disease contexts.

How does TCEAL7 interact with the transcriptional machinery to regulate gene expression?

TCEAL7 functions as a transcriptional regulator, but its precise mechanism requires further investigation. Advanced research should focus on:

• Protein complex analysis:

  • Immunoprecipitation followed by mass spectrometry

  • Proximity labeling techniques (BioID, APEX) to identify transient interactions

  • ChIP-seq co-localization with transcriptional machinery components

• Mechanistic studies:

  • In vitro transcription assays with purified components

  • Analysis of RNA polymerase II phosphorylation status

  • Investigation of elongation rates on target genes

• Structural biology approaches:

  • Determination of TCEAL7 protein structure

  • Analysis of interaction interfaces with transcriptional machinery

  • Structure-function relationship studies using mutagenesis

Current evidence suggests TCEAL7 may regulate transcription by modulating Myc and NF-κB activity , but the direct molecular mechanisms remain to be fully elucidated.

What is the evolutionary significance of TCEAL7 conservation across species?

Understanding the evolutionary history of TCEAL7 can provide insights into its fundamental biological roles:

• Comparative genomics:

  • Analyze TCEAL7 orthologs across species

  • Identify conserved regulatory elements, particularly E-box motifs

  • Compare expression patterns in different vertebrate lineages

• Functional conservation:

  • Test whether TCEAL7 orthologs from different species can functionally substitute for human TCEAL7

  • Identify lineage-specific adaptations in TCEAL7 sequence and function

• Evolutionary pressure analysis:

  • Calculate selection pressures on different TCEAL7 domains

  • Identify rapidly evolving regions that may indicate species-specific functions

These evolutionary analyses can help researchers distinguish fundamental TCEAL7 functions from species-specific adaptations.

How does TCEAL7 coordinate with other factors to regulate cell fate decisions?

TCEAL7 plays a role in cellular differentiation, particularly in muscle development . Advanced research questions should address:

• Temporal coordination:

  • Precise timing of TCEAL7 induction during differentiation

  • Relationship to cell cycle exit and commitment to differentiation

  • Sequential interactions with other regulatory factors

• Pathway integration:

  • How TCEAL7 integrates signals from multiple pathways

  • Cross-talk with other transcriptional regulators

  • Feedback mechanisms that stabilize cell fate decisions

• Single-cell heterogeneity:

  • Variation in TCEAL7 expression among seemingly identical cells

  • Role in determining which cells differentiate versus maintain proliferative capacity

  • Relationship to cellular memory and epigenetic states

Current research indicates that TCEAL7 overexpression decreases cellular proliferation and enhances differentiation, with p27 upregulation being one potential mechanism . This suggests TCEAL7 may function as a molecular switch in cell fate determination.