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- Table of Contents
Facts about G-rich sequence factor 1.
Preferentially binds RNAs transcribed from three contiguous genes on the light strand of mtDNA, the ND6 mRNA, and the long non-coding RNAs for MT-CYB and MT-ND5, each of which contains multiple consensus binding sequences. .
Human | |
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Gene Name: | GRSF1 |
Uniprot: | Q12849 |
Entrez: | 2926 |
Belongs to: |
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No superfamily |
FLJ13125; G-rich RNA sequence binding factor 1; G-rich sequence factor 1; GRSF-1
Mass (kDA):
53.126 kDA
Human | |
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Location: | 4q13.3 |
Sequence: | 4; NC_000004.12 (70815783..70843274, complement) |
[Isoform 1]: Mitochondrion matrix. Localizes to mitochondrial RNA granules found in close proximity to the mitochondrial nucleoids.; [Isoform 2]: Cytoplasm.
G-rich sequence factors 1 (GRSF1) are a post-transcriptional controller for mitochondrial gene expression. It is required for the assembly of the mitochondrial ribosome as well as the recruitment of lncRNA and mRNA. This marker is utilized by scientists in numerous applications including biotechnology and animal healthcare. It is useful to all scientists across the globe.
GRSF1 has been proven to promote cancer and EMT-mediated metastasis. Additionally this cellular protein has been found to be linked to a PI3K/AKT signaling pathway and can promote senescence. Furthermore, loss of GRSF1 increases mTOR activity and activates the proinflammatory transcriptional pathway in various cancers. GRSF1 is also a key age-related regulator of the process of senescence. A new miRNA was identified to drive cervical cancer cell metastasis using NFKappab/PIK3R3/AKT.
Prior to this, we had reported that GRSF1 is an antagonist of the senescent marker, HuR, in human fibroblasts. Human fibroblasts show significantly lower levels of GRSF1 expression than cells without PD. Similar results were observed in adriamycin caused senescent liposarcoma cell, and adriamycin inducing human skin fibroblasts. GRSF1 expression is also negatively affected by DNA methylation.
Numerous studies have revealed that GRSF1 regulates the expression of genes in mitochondria. The mitochondria are involved in catabolic metabolism (breakdown of macromolecules that are large in the presence of energy) and anabolic metabolism (production of large macromolecules by the use of small metabolic intermediates that require energy).
The GRSF1 enzyme is involved in the regulation of beta-secretase activity in neurons. It performs a variety of functions and is a frequent component of Alzheimer's disease. It is also a crucial component in the rapid feed-forward regulatory system of beta-secretase. These studies also show that GRSF1 regulates mRNA translation.
GRSF1 is responsible for mitochondrial replication and regulates the expression of post-transcriptional genes. Different levels of POLRMT expression lead to different metabolic effects. This is what makes POLRMT an attractive therapeutic target. Although there aren't any drugs currently that target GRSF1, POLRMT is a essential player in these processes.
The GRSF1 receptor binds to RMRP as a part of the RNA-processing endoribonuclease enzyme, which is found in mitochondria. RMRP is essential for the activity of enzymatic enzymes, as the RNase MRP cleaves mitochondrial DNA at a specific site. This location marks the transition between primer RNA synthesis and DNA synthesis. It also serves as the primary source of mitochondrial DNA replication. Researchers concluded that GRSF1 was linked to mitochondrial bioenergetics and mitochondrial apoptosis.
The GRSF1 gene encodes two isoforms. Isoform 1 is a mitochondrial polynucleotide-phosphorylase, an RNA-processing enzyme. Both areoforms contain three RNA binding motif and an indication of mitochondrial localization. The GRSF1 is a preferred mRNA binding molecule that contain contiguous genes on the light mitochondrial DNA. GRSF1 regulates mitochondrial RNA processing as well as post-transcriptional storage.
In addition to its role in lncRNAs encoded by mtDNA, GRSF1 has been implicated in the development of a variety of cancers. These tumors contain a significant ia revealed thsm hs teakdoRMT expreedll, ann thdoRMT expre reveals teakbl larkgrowthis. Id cat alsinhibital l pos cellulaf cancbe.
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