MIR29A

gene
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Also known as hsa-mir-29hsa-mir-29a

Summary

MIR29A (microRNA 29a, HGNC:31616) is a microRNA gene on chromosome 7q32.3.

microRNAs (miRNAs) are short (20-24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. miRNAs are transcribed by RNA polymerase II as part of capped and polyadenylated primary transcripts (pri-miRNAs) that can be either protein-coding or non-coding. The primary transcript is cleaved by the Drosha ribonuclease III enzyme to produce an approximately 70-nt stem-loop precursor miRNA (pre-miRNA), which is further cleaved by the cytoplasmic Dicer ribonuclease to generate the mature miRNA and antisense miRNA star (miRNA*) products. The mature miRNA is incorporated into a RNA-induced silencing complex (RISC), which recognizes target mRNAs through imperfect base pairing with the miRNA and most commonly results in translational inhibition or destabilization of the target mRNA. The RefSeq represents the predicted microRNA stem-loop.

Source: NCBI Gene 407021 — RefSeq curated summary.

At a glance

  • Gene type: non-coding (miRNA) — no protein product; not a drug target. Variant/disease associations are omitted (they would be positional, from an overlapping protein-coding gene).

Identifiers

Gene identifiers

FieldValue
HGNC IDHGNC:31616
Approved symbolMIR29A
NamemicroRNA 29a
Location7q32.3
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-29, hsa-mir-29a
Ensembl geneENSG00000284032
Ensembl biotypemiRNA
OMIM610782
Entrez407021
RNAcentralURS00004E9304 — miRNA, 64 nt, 31 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000362111

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000362111 — 1 exons

ExonStartEnd
ENSE00001436874130876747130876810

Expression profiles

Bgee: expression breadth broad, 81 present calls, max score 94.83.

Top tissues by expression

81 total, by Bgee expression score (0-100, higher = more expressed):

TissueAnatomy IDExpression scoreQuality
epididymisUBERON:000130194.83gold quality
adrenal tissueUBERON:001830388.44gold quality
midbrainUBERON:000189186.95gold quality
sural nerveUBERON:001548885.93gold quality
bone marrowUBERON:000237185.85gold quality
olfactory segment of nasal mucosaUBERON:000538685.52gold quality
vermiform appendixUBERON:000115484.93gold quality
calcaneal tendonUBERON:000370182.40gold quality
kidneyUBERON:000211382.21gold quality
liverUBERON:000210779.72gold quality
bloodUBERON:000017879.19gold quality
renal glomerulusUBERON:000007479.05gold quality
placentaUBERON:000198778.65gold quality
muscle of legUBERON:000138377.83gold quality
body of stomachUBERON:000116176.23gold quality
right lobe of liverUBERON:000111475.92gold quality
stomachUBERON:000094575.78gold quality
gastrocnemiusUBERON:000138873.17gold quality
islet of LangerhansUBERON:000000672.32gold quality
right atrium auricular regionUBERON:000663172.31gold quality
descending thoracic aortaUBERON:000234572.06gold quality
gall bladderUBERON:000211071.72gold quality
heartUBERON:000094870.96gold quality
right ovaryUBERON:000211870.89gold quality
monocyteCL:000057670.87gold quality
endometriumUBERON:000129570.74gold quality
body of pancreasUBERON:000115070.38gold quality
omental fat padUBERON:001041469.84gold quality
right adrenal gland cortexUBERON:003582769.84gold quality
tibial arteryUBERON:000761069.50gold quality

Single-cell (SCXA)

Detected in 1 experiment(s), a significant marker in 0.

ExperimentMarker?Max mean expression
E-ANND-3no1.47

Regulation

Is transcription factor: no

Upstream regulators (CollecTRI, top): NR1H4, PPARG

Literature-anchored findings (GeneRIF, showing 40)

  • MIRN29A(microRNA 29a) is one of the human microRNAs which target the nef trsnacript in HIV-1 as evidenced by computational predictions. (PMID:16236258)
  • Loss of specific miRNAs can contribute to increased BACE1 and Abeta levels in sporadic Alzheimer’s disease. (PMID:18434550)
  • miR-29 acts as a regulator of cardiac fibrosis and represents a potential therapeutic target for tissue fibrosis in general. (PMID:18723672)
  • miR-29 is epigenetically silenced by an activated NF-kappaB-YY1 pathway and is associated with rhabdomyosarcoma. (PMID:18977326)
  • Cellular miRNA hsa-miR29a downregulates the expression of Nef protein and interferes with HIV-1 replication. (PMID:19102781)
  • down regulation of miR-34a, miR-29 and miR-17-5p in aggressive CLL with TP53 abnormalities (PMID:19347736)
  • Data showed that miR-29a negatively regulated collagen IV by directly targeting the 3’UTRs of col4a1 and col4a2. (PMID:20067797)
  • miR-29 inhibits CDK6 protein & mRNA levels by direct binding to 3’-untranslated region. Down-regulation of miR-29 could cooperate with cyclin D1 in mantle-cell lymphoma pathogenesis. (PMID:20086245)
  • Our data indicate that miR-29a regulates early hematopoiesis and suggest that miR-29a initiates acute myeloid leukemia by converting myeloid progenitors into self-renewing leukemia stem cells (PMID:20212066)
  • Data demonstrate that miR-29 and Wnt signaling are involved in a regulatory circuit that can modulate osteoblast differentiation. (PMID:20551325)
  • Results indicate that in addition to c-Myc, mir-29b-1/mir-29a expression can be suppressed by hedgehog signaling and inflammatory pathways, both commonly activated in the genesis of malignancies. (PMID:20564213)
  • Data showed miR-29a expression was 4.5-fold higher in indolent CLL than in normal CD19+ B cells, whereas aggressive CLL samples showed a 3.2-fold increase. (PMID:20566844)
  • Data show that t(6;7)(p25.3;q32.3) was associated with down-regulation of DUSP22 and up-regulation of MIR29 microRNAs on 7q32.3. (PMID:21030553)
  • miR-29 and miR-30 regulate B-Myb expression by binding to its 3’UTR; these microRNAs play an important role in Rb-driven cellular senescence (PMID:21187425)
  • The findings derived from this study identify the miR-29 family as a critical regulator of ECM expression in the TM and suggest that its modulation by TGF-beta2 may be important in controlling ECM synthesis. (PMID:21330653)
  • Synthetic miR-29a represents a potential new tool to affect tumorigenesis in these lymphomas. (PMID:21471522)
  • methylation-dependent tissue-specific regulation of the lncRNA MEG3 by miR-29a may contribute to hepatocellular cancer growth. (PMID:21625215)
  • miR-29a, miR-29b selectively target MCT1 3’UTR ; the miR-29 isoforms are highly expressed in islets and contribute to silencing Mct1 in beta cells; miR-29 isoforms contribute to beta-cell-specific silencing of the MCT1 transporter and may affect insulin release (PMID:21646425)
  • miR-29a and miR-142-3p are downregulated in acute myeloid leukemia and have potential value as molecular diagnostic markers. (PMID:21678057)
  • the regulatory relationship between miRNAs and the p42.3 gene (PMID:21998710)
  • A significant inverse relationship between miR-29a and total MMP-2 was identified in the thoracic aortic aneurysm specimens. (PMID:22010139)
  • Findings suggest that serum miR-29a has strong potential as a novel noninvasive biomarker for early detection of CRC with liver metastasis. (PMID:22018950)
  • MiR29 suppresses DNMT activity and thus induces expression of COX2 and PGE2 during influenza A virus infection. (PMID:22072783)
  • miR-29 antagonism may promote increased elastin levels during conditions of elastin deficiencies. (PMID:22095981)
  • an increase of miR-29a, and hence decrease of Nasp, may contribute to inhibit cell proliferation during postnatal organ development. (PMID:22194605)
  • miR-29a/c could be potential biomarkers for colorectal cancer early recurrence. (PMID:22348113)
  • There is a significant impact of miR-29a on the risk of recurrence in patients with stage II but not in patients with stage I colon cancer. (PMID:22426940)
  • miR-29a and miR-142-3p are key regulators of normal myeloid differentiation and their reduced expression is involved in acute myeloid leukemia development. (PMID:22493297)
  • The expression of miR-29a in serum was significantly increased in patients with multiple myeloma compared to healthy donors. (PMID:22712836)
  • MiR-29 expression is suppressed by progestins in breast cancer cells. (PMID:22751119)
  • we demonstrate that loss of endogenous miR-29, derived from the miR-29ab1 genomic cluster, results in unrestrained T-bet expression and IFN-gamma production (PMID:22772450)
  • summarize current knowledge on the genomic organization and regulation of the miR-29 family and we provide an overview of its implication in cancer suppression and promotion as well as in host immune responses (PMID:22934851)
  • miR-29a up-regulation is involved in glucose-induced proliferation of beta-cells. (PMID:22940552)
  • analysis of novel targets for miR-29a using miRNA proteomics (PMID:22952654)
  • down-regulation of miR-29a was associated with advanced clinical features and poor prognosis of the pediatric acute myeloid leukemia patients (PMID:22981932)
  • Expression of miR-29a is important in the regulation of the SPARC gene expression and hepatocellular carcinoma growth. (PMID:23023935)
  • Low MIRN29 expression is associated with multiple myeloma. (PMID:23100393)
  • data obtained highlight the role of miRNA-29a in the regulation of osteoblastic cell apoptosis by silencing Bcl-2 and Mcl-1 and inducing E2F1 and E2F3 expression. (PMID:23113351)
  • Data show that miR-29 acts via 4 target sites within the RNASEL 3’ UTR. (PMID:23113544)
  • Elevated expression of miR-29 may play an important role in the pathogenesis of diseases related to fibrogenic reactions in human lung fibroblasts. (PMID:23238947)

Cross-species orthologs

2 orthologs

OrganismSymbolGene ID
danio_reriomir29a-1ENSDARG00000081841
mus_musculusMir29aENSMUSG00000065610

Paralogs (3): MIR29B1 (ENSG00000283797), MIR29B2 (ENSG00000284203), MIR29C (ENSG00000284214)

Protein

Non-coding RNA — no protein product; not a drug target.

Function

No curated pathway, Gene-Ontology, or interaction data.

Disease & clinical

No curated disease, variant, or cancer-driver associations.

Drugs & pharmacology

No drug or pharmacology data — not an established drug target.

No linked Atlas pages yet — the cross-entity mesh grows as the corpus expands.