関: resolvase

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2017/07/16 18:33:50」(JST)

wiki en

Recombinases are genetic recombination enzymes. DNA recombinases are widely used in multicellular organisms to manipulate the structure of genomes, and to control gene expression. These enzymes, derived from bacteria and fungi, catalyze directionally sensitive DNA exchange reactions between short (30–40 nucleotides) target site sequences that are specific to each recombinase. These reactions enable four basic functional modules, excision/insertion, inversion, translocation and cassette exchange, which have been used individually or combined in a wide range of configurations to control gene expression.^[1]^[2]^[3]^[4]^[5]

Types include:

Cre recombinase
Hin recombinase
Tre recombinase
FLP recombinase

References

^ Nern, A; Pfeiffer, BD; Svoboda, K; Rubin, GM (Aug 23, 2011). "Multiple new site-specific recombinases for use in manipulating animal genomes.". Proceedings of the National Academy of Sciences of the United States of America. 108 (34): 14198–203. PMC 3161616 . PMID 21831835. doi:10.1073/pnas.1111704108.
^ García-Otín, AL; Guillou, F (Jan 1, 2006). "Mammalian genome targeting using site-specific recombinases.". Frontiers in Bioscience. 11: 1108–36. PMID 16146801. doi:10.2741/1867.
^ Dymecki, SM; Kim, JC (Apr 5, 2007). "Molecular neuroanatomy's "Three Gs": a primer.". Neuron. 54 (1): 17–34. PMC 2897592 . PMID 17408575. doi:10.1016/j.neuron.2007.03.009.
^ Luan, H; White, BH (Oct 2007). "Combinatorial methods for refined neuronal gene targeting.". Current Opinion in Neurobiology. 17 (5): 572–80. PMID 18024005. doi:10.1016/j.conb.2007.10.001.
^ Fenno, LE; Mattis, J; Ramakrishnan, C; Hyun, M; Lee, SY; He, M; Tucciarone, J; Selimbeyoglu, A; Berndt, A; Grosenick, L; Zalocusky, KA; Bernstein, H; Swanson, H; Perry, C; Diester, I; Boyce, FM; Bass, CE; Neve, R; Huang, ZJ; Deisseroth, K (Jul 2014). "Targeting cells with single vectors using multiple-feature Boolean logic.". Nature Methods. 11 (7): 763–72. PMC 4085277 . PMID 24908100. doi:10.1038/nmeth.2996.

External links

Recombinases at the US National Library of Medicine Medical Subject Headings (MeSH)

This genetics article is a stub. You can help Wikipedia by expanding it.

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. マウス遺伝子：育種戦略と遺伝子工学 mouse genetics breeding strategies and genetic engineering
2. マントル細胞リンパ腫の病理学 pathobiology of mantle cell lymphoma
3. 多発血管炎性肉芽腫症（ウェゲナー肉芽腫症）を伴う肉芽腫症および関連血管炎の病因 pathogenesis of granulomatosis with polyangiitis wegeners and related vasculitides
4. 肝細胞移植 hepatocyte transplantation
5. 遺伝性乳癌・卵巣癌症候群の遺伝子検査 genetic testing for hereditary breast and ovarian cancer syndrome

English Journal

Protective role of vascular smooth muscle cell PPARγ in angiotensin II-induced vascular disease.

Marchesi C, Rehman A, Rautureau Y, Kasal DA, Briet M, Leibowitz A, Simeone SM, Ebrahimian T, Neves MF, Offermanns S, Gonzalez FJ, Paradis P, Schiffrin EL.SourceLady Davis Institute for Medical Research, Jewish General Hospital, McGill University, Montreal, Quebec, Canada.
Cardiovascular research.Cardiovasc Res.2013 Mar 1;97(3):562-70. doi: 10.1093/cvr/cvs362. Epub 2012 Dec 17.
AIMS: Vascular peroxisome proliferator-activated receptor γ (PPARγ) activation improves vascular remodelling and endothelial function in hypertensive rodents. The goal of this study was to determine that vascular smooth muscle cell (VSMC) PPARγ exerts a vascular protective role beyond its metabol
PMID 23250918

Interaction of the putative tyrosine recombinases RipX (UU145), XerC (UU222), and CodV (UU529) of Ureaplasma parvum serovar 3 with specific DNA.

Zimmerman CU, Rosengarten R, Spergser J.SourceInstitute of Bacteriology, Mycology and Hygiene, University of Veterinary Medicine Vienna, Vienna, Austria.
FEMS microbiology letters.FEMS Microbiol Lett.2013 Mar;340(1):55-64. doi: 10.1111/1574-6968.12077. Epub 2013 Jan 31.
Phase variation of two loci ('mba locus' and 'UU172 phase-variable element') in Ureaplasma parvum serovar 3 has been suggested as result of site-specific DNA inversion occurring at short inverted repeats. Three potential tyrosine recombinases (RipX, XerC, and CodV encoded by the genes UU145, UU222,
PMID 23305333

Reduction of mutant ataxin-7 expression restores motor function and prevents cerebellar synaptic reorganization in a conditional mouse model of SCA7.

Furrer SA, Waldherr SM, Mohanachandran MS, Baughn TD, Nguyen KT, Sopher BL, Damian VA, Garden GA, La Spada AR.AbstractSpinocerebellar ataxia type 7 (SCA7) is a dominantly inherited neurodegenerative disorder caused by a CAG - polyglutamine (polyQ) repeat expansion in the ataxin-7 gene. In polyQ disorders, synaptic dysfunction and neurodegeneration may develop prior to symptom onset. However, conditional expression studies of polyQ disease models demonstrate that suppression of gene expression can yield complete reversal of established behavioral abnormalities. To determine if SCA7 neurological and neurodegenerative phenotypes are reversible, we crossed PrP-floxed-SCA7-92Q BAC transgenic mice with a tamoxifen-inducible Cre recombinase transgenic line, CAGGS-Cre-ER™. PrP-floxed-SCA7-92Q BAC;CAGGS-Cre-ER™ bigenic mice were treated with a single dose of tamoxifen 1 month after the onset of detectable ataxia, which resulted in ∼50% reduction of polyQ-ataxin-7 expression. Tamoxifen treatment halted or reversed SCA7 motor symptoms, reduced ataxin-7 aggregation in Purkinje cells (PCs), and prevented loss of climbing fiber (CF)-PC synapses in comparison to vehicle-treated bigenic animals and tamoxifen-treated PrP-floxed-SCA7-92Q BAC single transgenic mice. Despite this phenotype rescue, reduced ataxin-7 expression did not result in full recovery of cerebellar molecular layer thickness or prevent Bergmann glia degeneration. These results demonstrate that suppression of mutant gene expression by only 50% in a polyQ disease model can have a significant impact on disease phenotypes, even when initiated after the onset of detectable behavioral deficits. The findings reported here are consistent with the emerging view that therapies aimed at reducing neurotoxic gene expression hold the potential to halt or reverse disease progression in afflicted patients, even after the onset of neurological disability.
Human molecular genetics.Hum Mol Genet.2013 Mar 1;22(5):890-903. doi: 10.1093/hmg/dds495. Epub 2012 Nov 29.
Spinocerebellar ataxia type 7 (SCA7) is a dominantly inherited neurodegenerative disorder caused by a CAG - polyglutamine (polyQ) repeat expansion in the ataxin-7 gene. In polyQ disorders, synaptic dysfunction and neurodegeneration may develop prior to symptom onset. However, conditional expression
PMID 23197655