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- Table of Contents
Facts about YTH domain-containing protein 1.
Acts as a key regulator of exon-inclusion or exon-skipping during alternative splicing via interaction with mRNA splicing factors SRSF3 and SRSF10 (PubMed:26876937). Specifically binds m6A-containing mRNAs and promotes recruitment of SRSF3 to its mRNA-binding elements adjacent to m6A sites, resulting in exon-inclusion during alternative splicing (PubMed:26876937).
Human | |
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Gene Name: | YTHDC1 |
Uniprot: | Q96MU7 |
Entrez: | 91746 |
Belongs to: |
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No superfamily |
YTH domain-containing protein 1
Mass (kDA):
84.7 kDA
Human | |
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Location: | 4q13.2 |
Sequence: | 4; NC_000004.12 (68310387..68350093, complement) |
Nucleus. Nucleus speckle. Localizes to a novel subnuclear structure, the YT bodies.
This article will discuss the ways in which YTHDC1 regulates autophagy. YTHDC1 not only regulates autophagy but also maintains sirtuin-1 mRNA stability and regulates mRNA nucleoport. This is how it plays a part in autophagy. This article will explain each of these processes, and how YTHDC1 can be used as a biomarker.
Although YTHDC1 is a well-studied component of cancer cells, it remains unclear what its function is. Zhang et.al. used TCGA data to screen differentially expressed RNA-binding proteins. This study shows that YTHDC1 expression significantly protects against bladder cell proliferation and metastasis. It may have a role in cancer development and progression as well.
Researchers have discovered that YTHDC1 regulates the nuclear export of m6A-modified chimeric mRNAs. This protein interacts directly with m6A and modulates the autophagy. These m6A readers play important roles in the progression of disease and in cellular functions. YTHDC1 a m6A important reader, as it regulates many biological functions, including cancer.
YTHDC1 is a co-receptor for YTHDF2, and plays an important role in cancer development. YTHDC1 facilitates the translation m6A modified mRNAs, while YTHDF3 blocks their degradation. These two proteins regulate the various functions within the ribosome.
YTHDC1 also plays a role as a catalyst for cancer progression. Hepatitis B virus infection (HBV) is the leading cause of hepatitis C. In hepatocellular tumor cells, YTHDC1 is known to regulate the translation m6A-modified circ -ARL3. This protein is essential for viral replication and has been implicated as a contributor to the development of hepatocellular carcinoma.
YTHDC1 in Drosophila regulates neuronal functions and sex determination. It also promotes the association of METTL3 with chromatin, which maintains the integrity of heterochromatin in embryonic stem cells and silences mammalian development retroviral elements. YTHDC1 can be decreased in keratinocytes. In diabetic mice, wound healing is delayed when SQSTM1 mRNA is not expressed.
The complex and dynamic relationship of m6A to autophagy is complex. Understanding their relationship may be helpful in developing new therapeutic strategies. The American Heart Association and other professional organizations have issued a scientific declaration regarding autophagy. However, the study does not prove conclusive. Further studies are needed to confirm this relationship. This is an important step in our quest to understand the underlying mechanisms behind autophagy.
YTHDC1 a subcellular adaptor protein that mediates target mRNA distribution. YTHDC1 not only maintains the stability of bound transcripts but also promotes the export these RNAs to the cytoplasm. This process is also observed using the RIPSeq assay. Its role in sirtuin stability mRNAs is unknown but could be important for understanding its functions.
Knocking down YTHDC1 reduces the infectivity of HIV-1 particles in the supernatant. It can alter the transcription and Env glycoprotein expression. It also inhibits trafficking and degradation CD4 in viral-producing cells. Moreover, it regulates the expression of Vpu and Env. This protein can be knocked down to prevent new infections.
YTHDC1 was a founding member in the YTH domain family. It promotes exon addition by recruiting SRSF3 in order to repel SRSF10. It interacts with the hnRNPA2B1, an RNA-binding protein that binds m6A-bearing DNA and modifies METTL3-mediated alternative Splicing Events. m6A influences RNA structure and makes it more accessible to hnRNPC/hnRNPG.
YTHDC1 regulates nuclear mRNA export by interacting with SRSF3, a component of the mRNA export pathway. Despite this association, SRSF3 doesn't confer biochemical selectivity on m6A in vitro. In vivo experiments have shown that knockdown YTHDC1 results in a decrease in the association between target mRNAs (and NXF1) These findings support the emerging regulatory capabilities of the nuclear mRNA-export machinery.
Previously, m6A was thought to affect gene expression post-transcriptionally, but the emerging evidence suggests that it also influences transcriptional control. METTL3 and YTHDC1 methylated chromosome-associated regulatory RNAs, and YTHDC1 reduced m6A methylation. This decreased methylation promoted transcription activity and chromatin accessibility.
The nuclear reader (YTHDC1) maintains sirtimun-1's mRNA stability and stability in vitro. It is responsible for viral RNA biogenesis and also regulates the expression of HIV-1 protein. These proteins cannot produce infectious viral particles efficiently without it. This study indicates that YTHDC1 plays a critical role in HIV-1 viral replication. It will be interesting to see how the depletion of YTHDC1 affects the stability of sirtuin 1 in vitro.
The downstream adaptor proteins form a functional protein -RNA complex together with mRNA and are capable of selective association to NXF1. The nucleus transforms the pgRNA to either rcDNA, or cccDNA. The mechanism by YTHDC1 regulating mRNA nuclear import is not clear. We conclude that YTHDC1 contributes to AML's oncogenicity.
The chemical marker m(6)A regulates how genetic information flows in different biological processes. In YTHDC1 knockdown cells, the m(6)A/A ratio of mRNA transcripts is decreased, and mRNAs accumulate in the nuclear region. However, knockdown cells do not have the YTHDF2 gene and express m6A-repeat mRNA.
YTHDC1 plays an important role in co-transcriptional regulation. It recruits KDM3B in order to promote H3K9me2 methylation in the m6A-associated areas of chromatin. It promotes KAP1 recruitment to targets of LINE1 scaffold. Additionally, it facilitates H3K9me3 trimethylation and transcription silencing. This protein contributes to embryonic and ESC identification.
To determine the function of YTHDC1 within ESCs, first we cloned Ythdc1 cKO ESCs. Then we transduced them using green fluorescent protein (GFP). We found that Ythdc1-cKO cells were less positive for GFP than Ythdc1-f/f ESCs. Moreover, YTHDC1 knockout mice showed no chimeras after being transduced using a green fluorescent protein(GFP).
The nucleus can transfer HBV RNAs into cells via a stepwise process. Pre-mRNAs have been packaged into messenger DNA protein complexes within the nucleus. Nuclear porous complexes facilitate the translocation of the targeted RNPs into cytoplasm. YTHDC1 and FMRP have been implicated in the nuclear export of HBV RNAs.
YTHDC1 & FMRP play a dual role in HBV's life cycle. Both proteins recognize m6A-methylated HBV transcripts and facilitate transport to the cytoplasm. Mutations of either of these proteins affect the viral life cycle. Deletion of YTHDC1 or FMRP affects cellular replication and the production of core-associated DNA.
Boster bio's YTHDC1 gene, a novel marker that regulates mRNA processing in autophagy, is a novel marker. The proper transport of mature transcripts species is dependent upon the YTHDC11 gene. It is located at junction of two exons. Researchers say that although it is rare, the YTHDC1 protein plays a significant function in this process.
The YTHDF3 gene is important for polarization of macrophages. To determine the role YTHDF3 played in M1 polarization, we infected macrophages by using fresh medium containing 100 ng/mL LPS and 50 ng/mL IFN-g. We collected the relevant samples and used them for future experiments.
The YTHDC1 mRNA interacts with ELAVL1/HuR mRNA to regulate autophagy. It also plays a key role in N6methyladenosine (RNA modification). The transcriptional regulator for SQSTM1 (an autophagy marker) is the YTHDC1 Gene. SQSTM1 plays an important role in the autophagic process. A knockout of this gene results in poor wound repair.
In a recent study, researchers found that knocking out YTHDC1 reduces the levels of viral proteins in producer cells. Unprocessed Env. gp160 is then incorporated into the virus particle. This results in decreased infectivity. To promote autophagy, the authors are currently working on a drug that targets SRSF3 and YTHDC1.
PMID: 12755701 by Wilkinson F.L., et al. Emerin interacts in vitro with the splicing-associated factor, YT521- B.
PMID: 19282290 by Heinrich B., et al. Heterogeneous nuclear ribonucleoprotein G regulates splice site selection by binding to CC(A/C)-rich regions in pre-mRNA.