Details for: MIR133A1HG

Gene ID: 102723167

Gene Type:  ncRNA (Non-coding RNA)  - A functional RNA molecule that is transcribed from DNA but not translated into a protein. Includes classes like miRNA and lncRNA.

Symbol: MIR133A1HG

Ensembl ID: ENSG00000265142

Description: MIR133A1 host gene

Selected Context(s):  Overall

Cell Significance Landscape

Contexts:

Associated with

Significant Cells

Cell Significance Index (CSI) scores for the chosen context(s)

  • fast muscle cell CL0000190
    CSI 3.02
    rCSI 11.8%
    PRS 97.88
  • cardiac muscle cell CL0000746
    CSI 2.3
    rCSI 3.3%
    PRS 98.85
  • regular atrial cardiac myocyte CL0002129
    CSI 1.92
    rCSI 6.19%
    PRS 99.32
  • regular ventricular cardiac myocyte CL0002131
    CSI 1.03
    rCSI 6.41%
    PRS 98.95

Cell ID: Standard Cell Ontology term used for mapping and comparing cells across experiments. Ensures consistency in analyzing cellular functions across tissues.
Fold Change: Represents the ratio of the current Cell Significance Index to the Cell Significance Index Threshold, indicating how much the gene expression has changed compared to a baseline.
Cell Significance Index: Reflects how strongly a gene is expressed in this specific cell.

Cell ID: Standard Cell Ontology term used for mapping and comparing cells across experiments. Ensures consistency in analyzing cellular functions across tissues.
Fold Change: Represents the ratio of the current Cell Significance Index to the Cell Significance Index Threshold, indicating how much the gene expression has changed compared to a baseline.
Cell Significance Index: Reflects how strongly a gene is expressed in this cell type. Calculated using techniques like effect size estimation and bootstrapping for reliability.

Cell ID: Standard Cell Ontology term used for mapping and comparing cells across experiments. Ensures consistency in analyzing cellular functions across tissues.
Fold Change: Represents the ratio of the current Cell Significance Index to the Cell Significance Index Threshold, indicating how much the gene expression has changed compared to a baseline.
Cell Significance Index: Reflects how strongly a gene is expressed in this cell type. Calculated using techniques like effect size estimation and bootstrapping for reliability.
Network Configuration

Explore relationships of the current gene. Select an Interaction Source: 'ONTOLOGY' for shared pathways (GO/Reactome) or 'STRING' for protein-protein interactions. Further refine by selecting context genes and comparing Cell Significance Index (CSI) scores between baseline and target cell types and their specific contexts.

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  • Node Color (Target Cell CSI, relative to current network):
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    • High
    • Medium
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    • Very Low
    • CSI N/A
  • Node Size: Proportional to Target Cell CSI magnitude
  • STRING PPI Edge
  • Shared Pathway Edge (ONTOLOGY)

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Other Information

This section provides additional information about the gene, including a description generated by an AI language model and details about associated proteins.

## Summary [MIR133A1HG](/details-gene/102723167) is a non-coding RNA gene located on chromosome 18q11.2, which functions as the host gene for the microRNA miR-133a-1. Its primary biological role involves post-transcriptional gene silencing through the RNA-induced silencing complex (RISC). Expression data indicates that [MIR133A1HG](/details-gene/102723167) is a highly significant and specific marker for muscle tissues, with its most prominent expression observed in [fast muscle cell](/details-cell/CL0000190)s and various types of [cardiac muscle cell](/details-cell/CL0000746)s, suggesting a fundamental role in myocyte biology. ## Cellular Roles and Expression Landscape The expression profile of [MIR133A1HG](/details-gene/102723167) demonstrates a highly specialized role in striated muscle cells. **Overall**, the gene shows the highest significance in [fast muscle cell](/details-cell/CL0000190) (CSI: 3.02), followed closely by [cardiac muscle cell](/details-cell/CL0000746) (CSI: 2.30), [regular atrial cardiac myocyte](/details-cell/CL0002129) (CSI: 1.92), and [regular ventricular cardiac myocyte](/details-cell/CL0002131) (CSI: 1.03). This restricted and high-level expression pattern strongly suggests that [MIR133A1HG](/details-gene/102723167) is a key molecular component in defining the identity and function of both skeletal and cardiac muscle lineages. Its consistent presence across different cardiomyocyte subtypes underscores its potential importance in maintaining fundamental cardiac physiology. ## Pathways and Molecular Function Functionally, [MIR133A1HG](/details-gene/102723167) is annotated with involvement in 'Mirna-mediated post-transcriptional gene silencing' ([GO:0035195](https://www.ebi.ac.uk/QuickGO/term/GO:0035195)). As a host gene, it gives rise to miR-133a, a microRNA that is incorporated into the [Risc complex](/details-cell/GO:0016442). Within this complex, miR-133a guides the silencing of target messenger RNAs, thereby regulating protein expression. This molecular function is critical in the context of muscle tissue, where precise control of gene expression is required for processes such as myoblast differentiation, muscle fiber type specification, and the hypertrophic response in cardiomyocytes. ## Research Directions The specific and high-level expression of [MIR133A1HG](/details-gene/102723167) in muscle cells points to its essential role in muscle development and disease. Its function in gene silencing makes it a pivotal regulator of cellular programs, and its dysregulation is likely implicated in myopathies and cardiac disorders. Based on the available data, several testable hypotheses can be proposed: 1. **Hypothesis:** [MIR133A1HG](/details-gene/102723167), via its product miR-133a, acts as a key regulator of cardiac muscle hypertrophy by targeting and suppressing the expression of pro-hypertrophic genes (e.g., *RhoA*, *Cdc42*). Downregulation of [MIR133A1HG](/details-gene/102723167) in cardiomyocytes may therefore be a causal factor in pathological cardiac remodeling. 2. **Hypothesis:** During skeletal muscle regeneration, the expression of [MIR133A1HG](/details-gene/102723167) is dynamically regulated to control the balance between myoblast proliferation and differentiation. Its upregulation may be required to silence proliferation-associated genes, thereby promoting terminal differentiation into mature [fast muscle cell](/details-cell/CL0000190)s. A key experiment to test the first hypothesis would be to use CRISPR interference (CRISPRi) to specifically suppress the transcription of [MIR133A1HG](/details-gene/102723167) in human induced pluripotent stem cell-derived cardiomyocytes ([iPSC-CMs](/details-cell/CL0002129)). Following suppression, these cells could be treated with a hypertrophic agonist like endothelin-1. The impact on cellular hypertrophy would be assessed by measuring cell surface area via high-content imaging, while target gene de-repression and downstream signaling pathway activation could be quantified using RNA-sequencing and western blotting. Given its muscle-specific expression and role as a master regulator, [MIR133A1HG](/details-gene/102723167) and its miRNA product represent a promising therapeutic avenue. For conditions like cardiac fibrosis or hypertrophy where miR-133a levels are often suppressed, a therapeutic strategy involving **activation** or supplementation would be appropriate. The delivery of synthetic miR-133a mimics, potentially encapsulated in nanoparticles targeted to cardiomyocytes, could restore normal gene regulation and ameliorate disease pathology. The high tissue specificity of the gene suggests that such a therapy would have a favorable safety profile with minimal off-target effects in non-muscle tissues.