GeneID: 453



Names

Common Name: miR-let-7d Type: Gene
Chromosome: 9 (NC_000009.12) Locus: NR_029481.1 (MIRLET7D)
HUGO Symbol: MIRLET7D Full Name: microRNA let-7d
Exons: N/A Introns: N/A

Description:
MicroRNAs (miRNAs), such as MIRNLET7D, are small, non-coding RNAs that play key roles in the post-transcriptional regulation of gene expression by targeting specific mRNAs. Let7, one of the founding members of the miRNA family, was first identified in C. elegans. There are several human homologs of C. elegans let7, including LET7D, and all of these LET7 miRNAs share an identical seed sequence critical for target recognition. MIRNLET7D plays a key role in the regulation of cellular iron homeostasis. It specifically and inversely regulates expression of the DMT1 ΔIRE isoform (a metal-iron transporter gene lacking an iron regulatory element), which controls the release of endosomal iron from transferrin into the cytoplasm for use by the cell. It also targets Bach1, a stress-responsive transcriptional factor that represses ferritin gene transcription, thereby de-repressing ferritin expression and increasing cellular iron storage via ferritin. Blood transfusion was shown to affect MIRNLET7D expression. In fact, MIRNLET7D expression was significantly lower in transfusion-dependent (TDT) β-thalassemia patients and was associated with excess iron in liver and cardiac tissues. It is postulated that MIRNLET7D could be a biomarker for cellular damage under condition of tissue iron excess.

Synonyms: LET7D , let-7d , MIRNLET7D , hsa-let-7d

Comments:
N/A

External Links

Sequence Viewer

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Publications / Origin

  1. Davis M, Clarke S, Influence of microRNA on the maintenance of human iron metabolism., Nutrients, 5(7), 2611-28, 2013 PubMed
  2. El-Khazragy N, Matbouly S, Hanna DH, Mahran NA, Mostafa SA, Abdelrehim BA, Farouk YK, Abuelela S, Circulating miRNAs and tissue iron overload in transfusion-dependent β-thalassemia major: novel predictors and follow-up guide., Ann Hematol, 2021 PubMed
Created on 2021-09-20 16:41:05, Last reviewed on (Show full history)


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