UVRAG: A Non-coding RNA Molecule Disrupting Gene Expression and Cell Division

Target Name: UVRAG

NCBI ID: G7405

UVRAG: A Non-coding RNA Molecule Disrupting Gene Expression and Cell Division

UVRAG, or UVA-associated gene regulatory network gene 5, is a non-coding RNA molecule that has been shown to play a crucial role in the regulation of gene expression in various organisms, including humans. One of the most significant functions of UVRAG is its ability to disrupt the process of heterotaxy, which is the process by which one cell type gives rise to another.

Heterotaxy is a critical process in the development and maintenance of tissues such as the brain, where new neurons are produced and different cell types are generated to replace those that are lost or damaged. However, when UVRAG is disrupted, this process becomes disrupted and can lead to a variety of diseases, including cancer.

One of the key mechanisms by which UVRAG disrupts heterotaxy is by binding to a protein called TATA-associated RNA-binding protein (TAS), which is a transcription factor that plays a critical role in the regulation of gene expression. When UVRAG binds to TAS, it can disrupt the formation of RNA-protein interactions, which are critical for the regulation of gene expression.

This disruption of TAS-RNA interactions can have a profound impact on gene expression and lead to the activation of genes that are involved in cell growth, survival, and reproduction. It is thought that UVRAG may be a drug target or biomarker for a variety of diseases, including cancer, due to its ability to disrupt the regulation of gene expression.

In addition to its role in the regulation of gene expression, UVRAG has also been shown to play a role in the regulation of cell division and the maintenance of stem cells. UVRAG has been shown to be involved in the regulation of the G1/S transition , which is a critical step in the cell cycle and is involved in the preparation of cells for cell division.

Furthermore, UVRAG has also been shown to play a role in the regulation of the G0/G1 transition, which is the stage of cell growth where cells prepare for cell division. UVRAG has also been shown to be involved in the regulation of cell cycle progression and in the maintenance of stem cells.

In conclusion, UVRAG is a non-coding RNA molecule that plays a critical role in the regulation of gene expression and cell division. Its disruption can lead to a variety of diseases, including cancer. UVRAG may be a drug target or biomarker for the treatment of these diseases. Further research is needed to fully understand the role of UVRAG in the regulation of gene expression and the development and maintenance of tissues.

Protein Name: UV Radiation Resistance Associated

Functions: Versatile protein that is involved in regulation of different cellular pathways implicated in membrane trafficking. Involved in regulation of the COPI-dependent retrograde transport from Golgi and the endoplasmic reticulum by associating with the NRZ complex; the function is dependent on its binding to phosphatidylinositol 3-phosphate (PtdIns(3)P) (PubMed:16799551, PubMed:18552835, PubMed:20643123, PubMed:24056303, PubMed:28306502). During autophagy acts as regulatory subunit of the alternative PI3K complex II (PI3KC3-C2) that mediates formation of phosphatidylinositol 3-phosphate and is believed to be involved in maturation of autophagosomes and endocytosis. Activates lipid kinase activity of PIK3C3 (PubMed:16799551, PubMed:20643123, PubMed:24056303, PubMed:28306502). Involved in the regulation of degradative endocytic trafficking and cytokinesis, and in regulation of ATG9A transport from the Golgi to the autophagosome; the functions seems to implicate its association with PI3KC3-C2 (PubMed:16799551, PubMed:20643123, PubMed:24056303). Involved in maturation of autophagosomes and degradative endocytic trafficking independently of BECN1 but depending on its association with a class C Vps complex (possibly the HOPS complex); the association is also proposed to promote autophagosome recruitment and activation of Rab7 and endosome-endosome fusion events (PubMed:18552835, PubMed:28306502). Enhances class C Vps complex (possibly HOPS complex) association with a SNARE complex and promotes fusogenic SNARE complex formation during late endocytic membrane fusion (PubMed:24550300). In case of negative-strand RNA virus infection is required for efficient virus entry, promotes endocytic transport of virions and is implicated in a VAMP8-specific fusogenic SNARE complex assembly (PubMed:24550300)

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