| 释义 |
- Inhibition of cell proliferation
- COL2A1 upregulation in Osteoarthritis
- See also
- References
- Further reading
- External links
{{Orphan|date=September 2012}}{{Infobox rfam
| Name = mir-675
| image =
| width =
| caption =
| Symbol = mir-675
| AltSymbols =
| Rfam = RF00897
| miRBase =
| miRBase_family = MIPF0000365
| RNA_type = microRNA
| Tax_domain = Eukaryota;
| GO =
| SO =
| CAS_number =
| EntrezGene =
| HGNCid =
| OMIM =
| PDB =
| RefSeq =
| Chromosome =
| Arm =
| Band =
| LocusSupplementaryData =
}}In molecular biology mir-675 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms. Inhibition of cell proliferationmiR-675 overexpression brings about reduced proliferation in a range of embryonic and extraembryonic stem cell lines. It has been found to be embedded in the first exon of the large intergenic non-coding RNA H19, which is responsible for limiting placental growth prior to birth. There is upregulation of the targets of miR-675 in placentas lacking H19; these include the insulin-like growth factor 1 receptor (IGF1R). Thus placentas lacking miR-675 continue to grow. It is possible that controlled miR-675 release from H19 may enable a rapid inhibition of cell proliferation in response to cellular stress or oncogenic signals.[1] COL2A1 upregulation in OsteoarthritismiR-675 has been found to be upregulated in osteoarthritic cartilage, alongside H19.[2] Indeed, there is co-regulation of these two RNAs. The COL2A1 gene associated with osteoarthritis through altered expression levels compared with in normal tissue is upregulated by miR-675 overexpression. It has been proposed that miR-675 may modulate collagen type II levels via an unknown target molecule, and there is potential for a diagnostic metabolic balance indicator in osteoarthritis through this microRNA. See also References 1. ^{{cite journal | vauthors = Keniry A, Oxley D, Monnier P, Kyba M, Dandolo L, Smits G, Reik W | title = The H19 lincRNA is a developmental reservoir of miR-675 that suppresses growth and Igf1r | journal = Nature Cell Biology | volume = 14 | issue = 7 | pages = 659–65 | date = June 2012 | pmid = 22684254 | pmc = 3389517 | doi = 10.1038/ncb2521 }}
2. ^{{cite journal | vauthors = Steck E, Boeuf S, Gabler J, Werth N, Schnatzer P, Diederichs S, Richter W | title = Regulation of H19 and its encoded microRNA-675 in osteoarthritis and under anabolic and catabolic in vitro conditions | journal = Journal of Molecular Medicine | volume = 90 | issue = 10 | pages = 1185–95 | date = October 2012 | pmid = 22527881 | pmc = | doi = 10.1007/s00109-012-0895-y | url = https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22527881 }}
Further reading {{refbegin}}- {{cite journal | vauthors = Xiao W, Bao ZX, Zhang CY, Zhang XY, Shi LJ, Zhou ZT, Jiang WW | title = Upregulation of miR-31 is negatively associated with recurrent/newly formed oral leukoplakia | journal = PLOS One | volume = 7 | issue = 6 | pages = e38648 | year = 2012 | pmid = 22719913 | pmc = 3377716 | doi = 10.1371/journal.pone.0038648 | editor1-last = Lo | editor1-first = Kwok-Wai }}
- {{cite journal | vauthors = Lu TX, Sherrill JD, Wen T, Plassard AJ, Besse JA, Abonia JP, Franciosi JP, Putnam PE, Eby M, Martin LJ, Aronow BJ, Rothenberg ME | title = MicroRNA signature in patients with eosinophilic esophagitis, reversibility with glucocorticoids, and assessment as disease biomarkers | journal = The Journal of Allergy and Clinical Immunology | volume = 129 | issue = 4 | pages = 1064–75.e9 | date = April 2012 | pmid = 22391115 | pmc = 3466056 | doi = 10.1016/j.jaci.2012.01.060 }}
- {{cite journal | vauthors = Martinez-Sanchez A, Dudek KA, Murphy CL | title = Regulation of human chondrocyte function through direct inhibition of cartilage master regulator SOX9 by microRNA-145 (miRNA-145) | journal = The Journal of Biological Chemistry | volume = 287 | issue = 2 | pages = 916–24 | date = January 2012 | pmid = 22102413 | pmc = 3256897 | doi = 10.1074/jbc.M111.302430 }}
- {{cite journal | vauthors = Schmitz KJ, Helwig J, Bertram S, Sheu SY, Suttorp AC, Seggewiss J, Willscher E, Walz MK, Worm K, Schmid KW | title = Differential expression of microRNA-675, microRNA-139-3p and microRNA-335 in benign and malignant adrenocortical tumours | journal = Journal of Clinical Pathology | volume = 64 | issue = 6 | pages = 529–35 | date = June 2011 | pmid = 21471143 | pmc = 3099361 | doi = 10.1136/jcp.2010.085621 }}
- {{cite journal | vauthors = Dudek KA, Lafont JE, Martinez-Sanchez A, Murphy CL | title = Type II collagen expression is regulated by tissue-specific miR-675 in human articular chondrocytes | journal = The Journal of Biological Chemistry | volume = 285 | issue = 32 | pages = 24381–7 | date = August 2010 | pmid = 20529846 | pmc = 2915673 | doi = 10.1074/jbc.M110.111328 }}
- {{cite journal | vauthors = Tsang WP, Ng EK, Ng SS, Jin H, Yu J, Sung JJ, Kwok TT | title = Oncofetal H19-derived miR-675 regulates tumor suppressor RB in human colorectal cancer | journal = Carcinogenesis | volume = 31 | issue = 3 | pages = 350–8 | date = March 2010 | pmid = 19926638 | pmc = | doi = 10.1093/carcin/bgp181 }}
- {{cite journal | vauthors = Smits G, Mungall AJ, Griffiths-Jones S, Smith P, Beury D, Matthews L, Rogers J, Pask AJ, Shaw G, VandeBerg JL, McCarrey JR, Renfree MB, Reik W, Dunham I | title = Conservation of the H19 noncoding RNA and H19-IGF2 imprinting mechanism in therians | journal = Nature Genetics | volume = 40 | issue = 8 | pages = 971–6 | date = August 2008 | pmid = 18587395 | pmc = | doi = 10.1038/ng.168 }}
{{refend}} External links - {{Rfam|id=RF00897|name=mir-675 microRNA precursor family}}
{{genetics-stub}} 2 : MicroRNA|MicroRNA precursor families |