HPA038299
Anti-TMEM165 antibody produced in rabbit
Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution
别名:
Anti-GDT1, Anti-TMPT27, Anti-TPARL
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关于此项目
Conjugate:
unconjugated
Clone:
polyclonal
Application:
immunofluorescence
immunohistochemistry
immunohistochemistry
Species reactivity:
human
Citations:
4
Technique(s):
immunofluorescence: 0.25-2 μg/mL
immunohistochemistry: 1:1000-1:2500
immunohistochemistry: 1:1000-1:2500
Uniprot accession no.:
产品名称
Anti-TMEM165 antibody produced in rabbit, Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution
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)
immunofluorescence: 0.25-2 μg/mL
immunohistochemistry: 1:1000-1:2500
immunogen sequence
REGLKMSPDEGQEELEEVQAELKKKDEEFQRTKLLNGPGDVETGTSITVPQ
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Quality Level
Gene Information
human ... TMEM165(55858)
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.
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.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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:
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.
Immunogen
transmembrane protein 165 recombinant protein epitope signature tag (PrEST)
Other Notes
Corresponding Antigen APREST79746
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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存储类别
10 - Combustible liquids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
常规特殊物品
常规特殊物品
此项目有
Sophie Groux-Degroote et al.
The FEBS journal, 285(18), 3442-3463 (2018-08-02)
The Sda /Cad antigen reported on glycoconjugates of human tissues has an increasingly recognized wide impact on the physio-pathology of different biological systems. The last step of its biosynthesis relies on the enzymatic activity of the β1,4-N-acetylgalactosaminyltransferase-II (B4GALNT2), which shows
Angel Ashikov et al.
Human molecular genetics, 27(17), 3029-3045 (2018-06-08)
Genomics methodologies have significantly improved elucidation of Mendelian disorders. The combination with high-throughput functional-omics technologies potentiates the identification and confirmation of causative genetic variants, especially in singleton families of recessive inheritance. In a cohort of 99 individuals with abnormal Golgi
Amrita Khakurel et al.
Molecular biology of the cell, 32(17), 1594-1610 (2021-06-24)
The Golgi complex is a central hub for intracellular protein trafficking and glycosylation. Steady-state localization of glycosylation enzymes is achieved by a combination of mechanisms involving retention and recycling, but the machinery governing these mechanisms is poorly understood. Herein we
Farhana Taher Sumya et al.
Traffic (Copenhagen, Denmark), 24(2), 52-75 (2022-12-06)
Conserved Oligomeric Golgi (COG) complex controls Golgi trafficking and glycosylation, but the precise COG mechanism is unknown. The auxin-inducible acute degradation system was employed to investigate initial defects resulting from COG dysfunction. We found that acute COG inactivation caused a
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