更新于：2024-05-01

Dicer

dicer 1, ribonuclease III

更新于：2024-05-01

基本信息

别名

Dicer、dicer 1, ribonuclease III、DICER1

+ [7]

简介

Double-stranded RNA (dsRNA) endoribonuclease playing a central role in short dsRNA-mediated post-transcriptional gene silencing. Cleaves naturally occurring long dsRNAs and short hairpin pre-microRNAs (miRNA) into fragments of twenty-one to twenty-three nucleotides with 3' overhang of two nucleotides, producing respectively short interfering RNAs (siRNA) and mature microRNAs. SiRNAs and miRNAs serve as guide to direct the RNA-induced silencing complex (RISC) to complementary RNAs to degrade them or prevent their translation. Gene silencing mediated by siRNAs, also called RNA interference, controls the elimination of transcripts from mobile and repetitive DNA elements of the genome but also the degradation of exogenous RNA of viral origin for instance. The miRNA pathway on the other side is a mean to specifically regulate the expression of target genes.

关联

100 项与 Dicer 相关的临床结果

登录后查看更多信息

100 项与 Dicer 相关的转化医学

登录后查看更多信息

0 项与 Dicer 相关的专利（医药）

登录后查看更多信息

4,115

项与 Dicer 相关的文献（医药）

2024-02-16·Blood

Let-7 miRNAs repress HIC2 to regulate BCL11A transcription and hemoglobin switching.

Article

作者: Peng Huang ; Scott A Peslak ; Vanessa Shehu ; Cheryl A Keller ; Belinda M Giardine ; Junwei Shi ; Ross C Hardison ; Gerd A Blobel ; Eugene Khandros

The switch from fetal (HBG) to adult (HBB) -globin gene transcription in erythroid cells serves as a paradigm for a complex, clinically relevant developmental gene regulatory program. We previously identified HIC2 as a regulator of the switch by inhibiting the transcription of BCL11A, a key repressor of HBG production. HIC2 is highly expressed in fetal cells but the mechanism of its regulation is unclear. Here we report that HIC2 developmental expression is controlled by miRNAs, as loss of global miRNA biogenesis through DICER1 depletion leads to upregulation of HIC2 and HBG mRNA. We identified the adult-expressed let-7 miRNA as a direct posttranscriptional regulator of HIC2. Ectopic expression of let-7 in fetal cells lowered HIC2 levels while inhibition of let-7 in adult erythroblasts increased HIC2 production, culminating in decommissioning of a BCL11A erythroid enhancer and reduced BCL11A transcription. HIC2 depletion in let-7-inhibited cells restored BCL11A-mediated repression of HBG. Together these data establish that fetal hemoglobin silencing in adult erythroid cells is under the control of a miRNA mediated inhibitory pathway (let-7 ⊣ HIC2 ⊣ BCL11A ⊣ HBG).

2024-02-15·The American journal of surgical pathology

Pathogenic Somatic Mutation of DICER1 and Clinicopathological Features in Nasal Chondromesenchymal Hamartomas: A Series of Nine Cases.

Article

作者: Chunyan Hu ; Yifeng Liu ; Lan Lin ; Cuncun Yuan ; Duan Ma ; Qiang Huang

Nasal chondromesenchymal hamartoma (NCMH) is a rare benign polypoid mesenchymal tumor arising in the nasal cavity and/or paranasal sinuses. Recognizing these sporadic, rare lesions is crucial, as surgical complete removal of the mass is the common treatment approach. This retrospective study analyzed the demographics, symptoms, and imaging data of 9 patients diagnosed with NCMH between January 2017 and June 2023, possibly representing the largest single-center adult case cohort to date. Diagnostic techniques included nasal endoscopy, CT/MRI scan, immunohistological studies, and morphologic comparisons. Pathologic specimens were subjected to Sanger sequencing of exons 24 and 25 of DICER1. The average age of 9 cases was 24.4 years, and the oldest was 55 years. Four of the patients were children, ranging from 1 year old to 11 years old, with an average of 4.5 years. Nasal congestion is the most common registered symptom. Endoscopic findings showed that most patients had smooth pink neoplasms or polypoid masses in the nasal meatus. Radiologic scanning revealed soft-tissue density masses that occupied the nasal cavity. Histologically, the characteristic structure of NCMHs is immature cellular cartilage nodules and mature cartilage nodules distributed in a loose mucoid matrix. Five of the 9 patients had somatic DICER1 missense mutations. Four of the patients with DICER1-mutated NCMH exhibited a p.E1813 missense hotspot mutation. We also report a case of a rare p.P1836H missense mutation. The detected DICER1 somatic mutations provide compelling evidence of an association with the DICER1 tumor family. We emphasize the importance of pathologic consultation and the need for pathologists to accumulate experience in NCMH diagnosis to avoid misdiagnosis.

2024-02-15·BMJ case reports

DICER1-mutant sarcoma of the internal auditory canal.

Article

作者: Clarice Ho ; Vanessa Goodwill ; John Ross Crawford

项与 Dicer 相关的新闻（医药）

2023-04-18

·PRNewswire

Star Gala inspires record-breaking donations to support life-saving resources for Children's Minnesota cancer and blood disorders program

MINNEAPOLIS and ST. PAUL, Minn., April 17, 2023 /PRNewswire/ -- Children's Minnesota announced today that a record-breaking $2.36 million was raised at this year's Star Gala – one of the biggest nights of the year for the philanthropic community in the Twin Cities. The 31st annual Star Gala benefited the Children's Minnesota cancer and blood disorders program, the largest program of its kind in the Upper Midwest. The event, hosted by KARE 11's Belinda Jensen, brought business leaders, philanthropists and community members to The Depot in Minneapolis on Saturday, April 15 to raise vital funds that will be invested in life-saving resources, wrap-around services for patient families, and cutting-edge cancer and blood disorders research. "Our program offers advanced, individualized care for our patients because we know that not every cancer and blood disorder diagnosis is the same. We also have the largest clinical research staff in the region, and we participate in over 100 research studies, meaning our patients have access to innovative treatments before they're widely available," said Dr. Sue Kearney, medical director of the cancer and blood disorders program. "We are grateful for the generosity of our community. Their support of our program allows us to continue advancing the treatment of cancer and blood disorders and provide the highly specialized care that can get kids on the road to recovery." To support Children's Minnesota, visit ChildrensMN.org/StarGala. The cancer and blood disorders program at Children's Minnesota cares for more than 3,500 patients from infants to young adults each year, including more than 80 percent of Minnesota children with sickle cell disease or hemoglobinopathies and other hemophilia diagnoses. Children's Minnesota is a part of the Therapeutic Advances in Childhood Leukemia & Lymphoma (TACL) consortium, which offers eligible patients with recurrent leukemias and lymphomas access to early studies of new drugs. The program is also a member of the Pacific Pediatric Neuro-Oncology Consortium (PNOC), which is made up of 18 children's hospitals dedicated to improving the outcomes for children with brain and spinal cord tumors. In addition, Children's Minnesota is home to the International Ovarian and Testicular Stromal Tumor Registry and International Pleuropulmonary Blastoma/DICER1 Registry. The registries collect clinical and biological information about these rare tumors in order to improve treatment and screening. The Star Gala was made possible by presenting sponsor APi Group. Other top sponsors at this year's event include: Baird Private Wealth Management and Great Clips. About Children's Minnesota Children's Minnesota is one of the largest pediatric health systems in the United States and the only health system in Minnesota to provide care exclusively to children, from before birth through young adulthood. An independent and not-for-profit system since 1924, Children's Minnesota serves kids throughout the Upper Midwest at two free-standing hospitals, nine primary care clinics, multiple specialty clinics and seven rehabilitation sites. As The Kids ExpertsTM, Children's Minnesota is regularly ranked by U.S. News & World Report as a top children's hospital. Find us on Facebook @childrensminnesota or on Twitter and Instagram @childrensmn. Please visit childrensMN.org. SOURCE Children's Minnesota