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Merck
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主要文件

HPA043665

Sigma-Aldrich

Anti-MRPL3 antibody produced in rabbit

Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution

别名:

Anti-MRL3, Anti-RPML3, Anti-mitochondrial ribosomal protein L3

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About This Item

分類程式碼代碼:
12352203
人類蛋白質圖譜編號:
NACRES:
NA.41
共軛:
unconjugated
application:
IHC
無性繁殖:
polyclonal
物種活性:
human
citations:
4
技術:
immunoblotting: 0.04-0.4 μg/mL
immunohistochemistry: 1:500-1:1000

生物源

rabbit

品質等級

共軛

unconjugated

抗體表格

affinity isolated antibody

抗體產品種類

primary antibodies

無性繁殖

polyclonal

產品線

Prestige Antibodies® Powered by Atlas Antibodies

形狀

buffered aqueous glycerol solution

物種活性

human

技術

immunoblotting: 0.04-0.4 μg/mL
immunohistochemistry: 1:500-1:1000

免疫原序列

GKSGTWWDEHLSEENVPFIKQLVSDEDKAQLASKLCPLKDEPWPIHPWEPGSFRVGLIALKLGMMPLWTKDGQKHVVTLLQVQDCHVLKYTSKENCNGK

UniProt登錄號

運輸包裝

wet ice

儲存溫度

−20°C

目標翻譯後修改

unmodified

基因資訊

human ... MRPL3(11222)

一般說明

The gene MRPL3 (mitochondrial ribosomal protein L3) is mapped to human chromosome 3q22.1. It is nuclear encoded and is a large subunit protein of 39S subunit of 55S mitochondrial ribosome.

免疫原

mitochondrial ribosomal protein L3 recombinant protein epitope signature tag (PrEST)

應用

All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project and as a result, are supported by the most extensive characterization in the industry.

The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. We also provide Prestige Antibodies® protocols and other useful information.

生化/生理作用

Mutation in the MRPL3 (mitochondrial ribosomal protein L3) gene causes hypertrophic cardiomyopathy. It also results in psychomotor retardation, particularly due to defects in mitochondrial translation. In addition, mutation in MRPL3 might also be associated with autosomal dominant non-syndromic hearing loss (DFNA18).

特點和優勢

Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.

Every Prestige Antibody is tested in the following ways:
  • IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
  • Protein array of 364 human recombinant protein fragments.

聯結

Corresponding Antigen APREST84658

外觀

Solution in phosphate buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide.

法律資訊

Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany

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儲存類別代碼

10 - Combustible liquids

水污染物質分類(WGK)

WGK 1

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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Exome sequencing identifies MRPL3 mutation in mitochondrial cardiomyopathy.
Galmiche L, et al.
Human Mutation, 32, 1225-1231 (2011)
Thomas W O'Brien et al.
Gene, 354, 147-151 (2005-05-24)
The ancestral mitochondrial ribosome (70S) underwent major structural remodeling during the evolution of mammalian mitochondrial ribosomes (55S). Despite the loss of nearly half their RNA, 55S ribosomes are actually larger than bacterial ribosomes because of all the extra proteins they
Aurelio Reyes et al.
PLoS genetics, 16(7), e1008923-e1008923 (2020-08-01)
Mitochondrial translation defects can be due to mutations affecting mitochondrial- or nuclear-encoded components. The number of known nuclear genes involved in mitochondrial translation has significantly increased in the past years. RCC1L (WBSCR16), a putative GDP/GTP exchange factor, has recently been

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