Results 11 to 20 of about 8,581 (127)

Tracing the molecular route to progression in miRNA-biogenesis-defective thyroid lesions [PDF]

open access: yesJCI Insight
Germline and somatic changes in DICER1 and DGCR8 microprocessors confer risk of developing benign and malignant thyroid lesions, yet the molecular events driving malignant transformation remain unclear.
Anne-Sophie Chong   +22 more
doaj   +2 more sources

From DGCR8 expression analysis to diseased pathways in 22q11.2 deletion syndrome [PDF]

open access: yesFrontiers in Immunology
22q11.2 deletion syndrome (22q11.2DS) is the most prevalent microdeletion disorder, distinguished by markedly diverse clinical manifestations, with its underlying molecular mechanisms not yet fully elucidated.
Valentina Boz   +9 more
doaj   +2 more sources

Risk Factors for Melanoma Survival: DGCR8 as a Predictive Factor for Mortality in Young Patients [PDF]

open access: yesActa Dermato-Venereologica
MicroRNA-processing enzymes – Dicer and DGCR8 – have been found to be dysregulated in melanoma. This study investigated whether these microRNA-processing enzymes could be used as risk factors for mortality.
Fabiola Schafer   +6 more
doaj   +2 more sources

DICER1 and DGCR8 in thyroid tumorigenesis: miRNA biogenesis and histopathologic diversity [PDF]

open access: yesEuropean Thyroid Journal
This review examines the emerging roles of DICER1 and DGCR8, key components of the miRNA biogenesis pathway, in thyroid pathogenesis, with a particular focus on their association with oncocytic morphology.
Lia Rodrigues   +6 more
doaj   +2 more sources

DGCR8 regulates multiple processes of transcription coupled nucleotide excision repair [PDF]

open access: yesScientific Reports
Ultraviolet (UV) radiation is a major environmental factor that induces DNA lesions. Cells have evolved repair pathways, in which the transcription-coupled nucleotide excision repair (TC-NER) has a central role in removing the lesions.
Takaaki Watanabe   +5 more
doaj   +2 more sources

Disrupted miRNA Biogenesis Machinery Reveals Common Molecular Pathways and Diagnostic Potential in MDS and AML [PDF]

open access: yesBiomedicines
Background: Myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) are clonal stem cell disorders in which disrupted post-transcriptional regulation contributes to aberrant hematopoiesis and leukemic transformation.
Kenan Çevik   +5 more
doaj   +2 more sources

Regulation of the microprocessor by post-translational modifications [PDF]

open access: yesFrontiers in Cell and Developmental Biology
The Microprocessor is an essential protein complex that is responsible for the first processing step in the biogenesis of canonical microRNAs. The core of this complex is composed of two proteins, the ribonuclease III enzyme DROSHA and its double ...
Ka Weng Leong   +3 more
doaj   +2 more sources

CCDC137/DGCR8 axis promotes aerobic glycolysis in hepatocellular carcinoma via activation of the AKT/mTOR signaling pathway [PDF]

open access: yesEuropean Journal of Medical Research
Introduction Hepatocellular carcinoma (HCC) is a leading cause of global cancer fatality. Understanding its molecular mechanisms is crucial for developing effective treatments.
Zhiying Xu   +6 more
doaj   +2 more sources

DGCR8/miR-106 Axis Enhances Radiosensitivity of Head and Neck Squamous Cell Carcinomas by Downregulating RUNX3

open access: yesFrontiers in Medicine, 2020
Purpose: Head and neck squamous cell carcinoma (HNSCC) is the sixth most prevalent malignant tumor worldwide, and the radiotherapy effect is strongly associated with human papillomavirus (HPV) infection. Therefore, the aim of our study was to analyze the
Chunlin Zhang   +5 more
doaj   +1 more source

Genomic analysis suggests that mRNA destabilization by the microprocessor is specialized for the auto-regulation of Dgcr8.

open access: yesPLoS ONE, 2009
BackgroundThe Microprocessor, containing the RNA binding protein Dgcr8 and RNase III enzyme Drosha, is responsible for processing primary microRNAs to precursor microRNAs.
Archana Shenoy, Robert Blelloch
doaj   +1 more source

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