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Facts about Endoribonuclease Dicer.
SiRNAs and miRNAs serve as guide to direct the RNA- induced silencing complex (RISC) to complementary RNAs to degrade them or prevent their interpretation. Gene silencing mediated by siRNAs, also referred to as RNA interference, controls the removal of transcripts from mobile and repetitive DNA elements of the genome but also the degradation of exogenous RNA of viral origin for instance.
Human | |
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Gene Name: | DICER1 |
Uniprot: | Q9UPY3 |
Entrez: | 23405 |
Belongs to: |
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helicase family |
DCR1; dicer 1, double-stranded RNA-specific endoribonuclease; dicer 1, ribonuclease type III; Dicer; Dicer1, Dcr-1 homolog (Drosophila); EC 3.1.26; EC 3.1.26.-; EC 3.1.26.3; Helicase MOI; Helicase with RNase motif; helicase-moi; HERNADicer1, Dcr-1 homolog; K12H4.8-LIKE; KIAA0928endoribonuclease Dicer
Mass (kDA):
218.682 kDA
Human | |
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Location: | 14q32.13 |
Sequence: | 14; NC_000014.9 (95086228..95158263, complement) |
Cytoplasm.
There are a lot of things you should keep in mind when performing experiments using DICER1 to target the gene. This article will focus on the DICER1 marker as well as its optimization verification, as well as troubleshooting. With these suggestions you can conduct successful experiments with DICER1.
The identification of patients suffering from DICER1-associated tumors is the best application of the DICER1 marker. These tumors have common morphological characteristics: primitive round cells with poorly differentiated spindle cells, non-committed spindle cells, and/or chondroid nodules. They can develop in any organ system and are usually caused by the DICER1 gene mutation.
The DICER1 gene is an anti-tumor gene since it is linked to both gain-of-function and loss-of-function mutations. The gene has been proposed as a haploinsufficient tumor suppressor. This implies that one or both of the variants is sufficient to stop the progression of tumors. One or both of the alleles are essential to maintain the capacity of the cell.
DICER1 mutations are associated with both uterine adenosarcomas as well as cER. A case study demonstrated that 18 cases (95%) of cERMS, and seven cases (95 percent) of uterine adenosarcomas (95%) had germline DICER1 variants. This mutation is unique to cERMS and DICER1 mutations could help in the differential diagnosis. The problem of diagnosis could be resolved by careful analysis of morphological features.
As a potential therapeutic target for ovarian cancer DICER1-associated tumors share a common physical appearance and pathogenetic pathways. The DICER1 gene plays a critical role in branching morphogenesis in the lung and kidneys and lung, which are vital organs in the normal development. Embryonic death can result from the loss of one or both of the alleles.
In the 1980s in the 1980s, DICER1 gene was isolated from human ovarian tumors. This mutation is associated to an increased chance of developing the disease among women. It is also associated with a lower risk of developing cancer in women who have other genetic defects. This mutation is known to cause asymmetric cell growth. The mutation is located in the RNase IIIb domain. Further research is required to determine the role of DICER1 in ovarian cancer.
In two study groups, the DICER1 gene was associated with familial CN. Exon 23 was identified in one family while exon 25 was discovered in a different family. The mutation in this gene is associated with familial CN and CPDN. It is possible that the gene might also be linked with other diseases, which means that the DICER1 gene has a direct causal relationship with blindness.
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The DICER1 marker which is bound to DICER1 genes is a highly specific marker. Boster Bio has a range of anti-DICER antibodies for testing their specificity. These are designed for human use and react with DICER1 protein. In order to make use of them in studies, you can purchase blocking peptides or Recombinant proteins.
In humans, DICER1 may serve as a biomarker of the presence of a disease. Changes in the DICER1 gene encoding the E1813G change result in an oncogenic allele. Further studies will identify the subset of DICER1 carriers at highest risk of developing aggressive gynecologic tumors and PPBs of type II or III. However, these results are currently limited.
It is possible that the identical DICER1 mutation may manifest differently in different individuals. A sibling carrying the gene may develop multiple tumors. Another sibling might not have any tumors. Other factors, such as environmental and genetic factors, could be a contributing factor to the growth of tumors. Although these factors aren't fully understood, they could help researchers determine if the DICER1 gene is linked to tumors.
DICER1 is a protein that encodes an RNase III endonuclease that cleaves precursor microRNAs into active miRNAs. Mutations in DICER1 cause a change in the expression of mature 5p miRNAs as well as increased risk of developing various cancers. Although this protein is well-known to be involved in cancer, its exact function is not yet known.
PMID: 10786632 by Matsuda S., et al. Molecular cloning and characterization of a novel human gene (HERNA) which encodes a putative RNA-helicase.
PMID: 20615407 by Potenza N., et al. A novel splice variant of the human dicer gene is expressed in neuroblastoma cells.
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