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- 详细信息
- 文献和实验
- 技术资料
- 保存条件:
"-20°C/-80°C"
- 保质期:
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
- 英文名:
Customized Rat Atp5mpl Protein (in vitro E.coli)
- 库存:
200
- 供应商:
武汉华美生物工程有限公司
- 规格:
20ug
Alternative Name(s)
6.8 kDa mitochondrial proteolipidEditorial/Sponsord
EditorialUniprot ID
D3Z9R8Gene Names
Atp5mplOrganism
RatAASequence
MLQSFIKKVWVPMKPYYTQVYQEIWVGVGLMSLIVYKIRSADKRSKALKGCSPAHAHGHHExpression Region
1-60aaSequence Info
Full lengthSource
in vitro E.coliSource Notice
Mammalian cell expression systems and other species are available. Please inquire.Tag Info
InquireMW
InquireList Price
1330Purity
Greater than 85% as determined by SDS-PAGE.Storage Buffer
Tris/PBS-based buffer, 6% TrehaloseStorage
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself. Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.Endotoxin
Not Test. Endotoxin removal service is available for free upon you request.产品类型
Transmembrane-Protein备注
**产品信息可能有变动,请以官网信息为准
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文献和实验**产品信息可能有变动,请以官网信息为准
Purification of Mitochondria for Enzymes Involved in Nucleic Acid Transactions
had a molecular weight estimated at 66-68 kDa in rat liver (1 ) or 46 kDa in Xenopus oocytes (2 ); similarly, some early estimates of the size of mtDNA polymerase suggested that it was a homotetramer of 47-kDa subunits (3 ,4 ). Both the mtRNA polymerase
Analysis of Phospholipid Hydroperoxide Glutathione Peroxidase mRNA
(6 ). In contrast, the homology between GPX1 and GPX4 is less than 40%. There are two forms of GPX4: the long form (23 kDa) with a leader sequence for transportation to mitochondria, and the short form (20 kDa) or the non-mitochondrial form (7 ). Although GPX
Use of Rat Genomics for Investigating the Metabolic Syndrome
of the Brown Norway rat influenced several major metabolic risk factors for type 2 diabetes and provided evidence that spontaneous variation in the mitochondrial genome per se can promote systemic metabolic disturbances relevant to the pathogenesis of metabolic
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