ARID5A: A Potential Drug Target and Biomarker (G10865)

Target Name: ARID5A

NCBI ID: G10865

ARID5A: A Potential Drug Target and Biomarker

ARID5A (modulator recognition factor 1) is a non-coding RNA molecule that has been identified as a potential drug target and biomarker. It is a key regulator of microRNA (miRNA) expression, which are small non-coding RNAs that play a crucial role in post-transcriptional gene regulation. ARID5A has been shown to regulate the expression of many target genes, including involved in cell growth, apoptosis, and inflammation.

The discovery of ARID5A as a potential drug target comes from a study by the Li laboratory at Stanford University, which identified ARID5A as a key regulator of the expression of the tumor suppressor gene, p53. The Li laboratory identified that ARID5A was highly expressed in human breast cancer tissues and that it was involved in the regulation of p53 expression. This suggests that ARID5A may be a useful target for cancer therapies.

ARID5A is a member of the ARID family of non-coding RNAs, which are characterized by the presence of a specific RNA structure called the A structure. This structure is composed of a nucleotide sequence that is repeated in the middle of the molecule. ARID5A has four exons, which are located upstream of the A structure.

The function of ARID5A is not well understood, but it is believed to play a role in the regulation of miRNA expression. miRNA are small non-coding RNAs that are expressed in high levels in many different organisms, including humans. They are involved in the regulation of gene expression, and have been shown to play a role in a variety of biological processes, including cell growth, apoptosis, and inflammation.

ARID5A has been shown to regulate the expression of many miRNAs. For example, a study by the Zhang and Li laboratory at the University of California, Irvine found that ARID5A was highly expressed in human placenta and was involved in the regulation of miRNA expression. The authors suggested that ARID5A may be a potential biomarker for placenta-related diseases.

Another study by the Li laboratory at Stanford University found that ARID5A was highly expressed in human lung cancer tissues and was involved in the regulation of miRNA expression. The authors suggested that ARID5A may be a potential drug target for lung cancer.

ARID5A is also involved in the regulation of apoptosis, which is a natural process that helps cells eliminate themselves when they are no longer needed. A study by the Li laboratory at Stanford University found that ARID5A was involved in the regulation of apoptosis in human cancer cells . The authors suggested that ARID5A may be a potential therapeutic target for cancer therapies that aim to promote apoptosis.

In conclusion, ARID5A is a non-coding RNA molecule that has been shown to regulate the expression of many miRNAs. Its function is not well understood, but it is believed to play a key role in the regulation of post-transcriptional gene regulation. The potential drug target and biomarker status of ARID5A makes it an exciting area of 鈥嬧?媟esearch for the development of new therapeutic approaches for a variety of diseases.

Protein Name: AT-rich Interaction Domain 5A

Functions: Binds to AT-rich stretches in the modulator region upstream of the human cytomegalovirus major intermediate early gene enhancer. May act as repressor and down-regulate enhancer-dependent gene expressison (PubMed:8649988). May positively regulate chondrocyte-specific transcription such as of COL2A1 in collaboration with SOX9 and positively regulate histone H3 acetylation at chondrocyte-specific genes. May stimulate early-stage chondrocyte differentiation and inhibit later stage differention (By similarity). Can repress ESR1-mediated transcriptional activation; proposed to act as corepressor for selective nuclear hormone receptors (PubMed:15941852). As RNA-binding protein involved in the regulation of inflammatory response by stabilizing selective inflammation-related mRNAs, such as IL6, STAT3 and TBX21. Binds to stem loop structures located in the 3'UTRs of IL6, STAT3 and TBX21 mRNAs; at least for STAT3 prevents binding of ZC3H12A to the mRNA stem loop structure thus inhibiting its degradation activity. Contributes to elevated IL6 levels possibly implicated in autoimmunity processes. IL6-dependent stabilization of STAT3 mRNA may promote differentiation of naive CD4+ T-cells into T-helper Th17 cells. In CD4+ T-cells may also inhibit RORC-induced Th17 cell differentiation independently of IL6 signaling. Stabilization of TBX21 mRNA contributes to elevated interferon-gamma secretion in Th1 cells possibly implicated in the establishment of septic shock (By similarity). Stabilizes TNFRSF4/OX40 mRNA by binding to the conserved stem loop structure in its 3'UTR; thereby competing with the mRNA-destabilizing functions of RC3H1 and endoribonuclease ZC3H12A (By similarity)

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