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Key Documents

HPA043665

Sigma-Aldrich

Anti-MRPL3 antibody produced in rabbit

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

Synonym(s):

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

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About This Item

UNSPSC Code:
12352203
Human Protein Atlas Number:
HPA043665
NACRES:
NA.41

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

product line

Prestige Antibodies® Powered by Atlas Antibodies

form

buffered aqueous glycerol solution

species reactivity

human

technique(s)

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

immunogen sequence

GKSGTWWDEHLSEENVPFIKQLVSDEDKAQLASKLCPLKDEPWPIHPWEPGSFRVGLIALKLGMMPLWTKDGQKHVVTLLQVQDCHVLKYTSKENCNGK

UniProt accession no.

P09001

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... MRPL3(11222)

General description

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.

Immunogen

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

Application

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.

Biochem/physiol Actions

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).

Features and Benefits

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.

Linkage

Corresponding Antigen APREST84658

Physical form

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

Legal Information

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

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Storage Class Code

10 - Combustible liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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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
Lindsey Van Haute et al.
Nature communications, 14(1), 1009-1009 (2023-02-24)
Mutations in the mitochondrial or nuclear genomes are associated with a diverse group of human disorders characterized by impaired mitochondrial respiration. Within this group, an increasing number of mutations have been identified in nuclear genes involved in mitochondrial RNA biology.
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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