MIR641

gene
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Also known as hsa-mir-641

Summary

MIR641 (microRNA 641, HGNC:32897) is a microRNA gene on chromosome 19q13.2.

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 693226 — 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:32897
Approved symbolMIR641
NamemicroRNA 641
Location19q13.2
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-641
Ensembl geneENSG00000207631
Ensembl biotypemiRNA
Entrez693226
RNAcentralURS000075CBEE — miRNA, 99 nt, 1 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000384899

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000384899 — 1 exons

ExonStartEnd
ENSE000014999064028254340282641

Expression profiles

Bgee: expression breadth ubiquitous, 111 present calls, max score 95.59.

Top tissues by expression

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

TissueAnatomy IDExpression scoreQuality
right uterine tubeUBERON:000130295.59gold quality
adrenal tissueUBERON:001830394.65gold quality
olfactory segment of nasal mucosaUBERON:000538692.94gold quality
right hemisphere of cerebellumUBERON:001489087.62gold quality
cerebellar hemisphereUBERON:000224585.07gold quality
right ovaryUBERON:000211884.77gold quality
left ovaryUBERON:000211984.69gold quality
skeletal muscle tissueUBERON:000113484.22gold quality
body of uterusUBERON:000985384.10gold quality
pituitary glandUBERON:000000783.97gold quality
ovaryUBERON:000099283.93gold quality
myometriumUBERON:000129683.18gold quality
metanephros cortexUBERON:001053382.57gold quality
endometriumUBERON:000129581.86gold quality
right coronary arteryUBERON:000162581.86gold quality
adenohypophysisUBERON:000219681.71gold quality
urinary bladderUBERON:000125581.33gold quality
endocervixUBERON:000045881.18gold quality
left uterine tubeUBERON:000130381.16gold quality
fallopian tubeUBERON:000388980.97gold quality
Brodmann (1909) area 9UBERON:001354080.66gold quality
left lobe of thyroid glandUBERON:000112080.40gold quality
kidneyUBERON:000211380.06gold quality
thyroid glandUBERON:000204679.91gold quality
muscle of legUBERON:000138379.65gold quality
lower esophagus muscularis layerUBERON:003583379.61gold quality
stomachUBERON:000094579.59gold quality
brainUBERON:000095579.53gold quality
lower esophagusUBERON:001347379.52gold quality
prefrontal cortexUBERON:000045179.51gold quality

Single-cell (SCXA)

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

ExperimentMarker?Max mean expression
E-ANND-3no0.39

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 13)

  • Our findings suggest that increased expression of miR-641 significantly contributes to erlotinib resistance development in NSCLC cells through activating ERK signaling by targeting NF1 and that inhibition of miR-641 may reverse acquired resistance of NSCLC cells to erlotinib treatment. (PMID:29493886)
  • CRNDE level was upregulated in NSCLC, and its knockdown suppressed NSCLC cells proliferation and enhanced apoptosis, whereas miR-641 antagonized the regulatory effect of CRNDE knockdown by directly binding to CRNDE. (PMID:30982057)
  • These results demonstrated that overexpression of TUSC8 could inhibit the invasion and migration of cervical cancer cells by upregulating PTEN via miR-641. (PMID:31033083)
  • Long non-coding RNA OIP5-AS1 promotes proliferation of gastric cancer cells by targeting miR-641. (PMID:31858545)
  • Circular RNA CDR1as Exerts Oncogenic Properties Partially through Regulating MicroRNA 641 in Cholangiocarcinoma. (PMID:32423991)
  • Long non-coding RNA LINC01963 inhibits progression of pancreatic carcinoma by targeting miR-641/TMEFF2. (PMID:32559621)
  • Circular RNA S-7 promotes ovarian cancer EMT via sponging miR-641 to up-regulate ZEB1 and MDM2. (PMID:32667627)
  • Circular RNA circSETD3 hampers cell growth, migration, and stem cell properties in bladder cancer through sponging miR-641 to upregulate PTEN. (PMID:34288821)
  • miR-641 Inhibited Cell Proliferation and Induced Apoptosis by Targeting NUCKS1/PI3K/AKT Signaling Pathway in Breast Cancer. (PMID:35069784)
  • LINC00665 sponges miR-641 to promote the progression of breast cancer by targeting the SNF2-related CREBBP activator protein (SRCAP). (PMID:35152838)
  • MiR-641 Exacerbates the Progression of Ischemic Stroke Through the MCL-1/Wnt/beta-Catenin Pathway. (PMID:35975488)
  • Long noncoding RNA SNHG1 promotes breast cancer progression by regulating the miR-641/RRS1 axis. (PMID:38331968)
  • The miR-641-STIM1 and SATB1 axes play important roles in the regulation of the Th17/Treg balance in ITP. (PMID:38755179)

Cross-species orthologs

0 orthologs

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.