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HPA019077

Sigma-Aldrich

Anti-DLEC1 antibody produced in rabbit

enhanced validation

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

Synonyme(s) :

Anti-CFAP81, Anti-DLC1

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100 μL
540,00 €

540,00 €


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100 μL
540,00 €

About This Item

Code UNSPSC :
12352203
Numéro HPA (Human Protein Atlas):
Nomenclature NACRES :
NA.43

540,00 €


Veuillez contacter notre Service Clients pour connaître la disponibilité de ce produit.

Source biologique

rabbit

Niveau de qualité

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Gamme de produits

Prestige Antibodies® Powered by Atlas Antibodies

Forme

buffered aqueous glycerol solution

Espèces réactives

human

Validation améliorée

orthogonal RNAseq
Learn more about Antibody Enhanced Validation

Technique(s)

immunofluorescence: 0.25-2 μg/mL
immunohistochemistry: 1:200-1:500

Séquence immunogène

PPVKSVSRWCIDSELLRKHHLISPEDYYTDTVPFHSAPKGISLPGCSKLTFSCEKRSVQKKELNKKLEDSCRKKLAEFEDELDHTVDSLTWNLTPKAKERTREPLKKASQPRN

Numéro d'accès UniProt

Conditions d'expédition

wet ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... DLEC1(9940)

Description générale

The gene DLEC1 (deleted in lung and esophageal cancer protein 1) is mapped to human chromosome 3p21.3. The protein localizes in the cytoplasm. DLEC1 is also called as DLC1 (deleted in lung cancer protein 1).

Immunogène

Deleted in lung and esophageal cancer protein 1 recombinant protein epitope signature tag (PrEST)

Application

Anti-DLEC1 antibody produced in rabbit, a Prestige Antibody, is developed and validated by the Human Protein Atlas (HPA) project . Each antibody is tested by immunohistochemistry against hundreds of normal and disease tissues. These images can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. The antibodies are also tested using immunofluorescence and western blotting. To view these protocols and other useful information about Prestige Antibodies and the HPA, visit sigma.com/prestige.

Actions biochimiques/physiologiques

DLEC1 (deleted in lung and esophageal cancer protein 1) is involved in growth suppression. It is down-regulated in ovarian cancer, nasopharyngeal cancer, gastric cancer, head and neck squamous cell carcinoma, non-small-cell lung cancer and renal cell carcinoma. Presence of DLEC1 results in suppression of tumor growth and reduces the invasiveness of cancer cells.

Caractéristiques et avantages

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.

Liaison

Corresponding Antigen APREST74732

Forme physique

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

Informations légales

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

Clause de non-responsabilité

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.

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Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

WGK 1

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Équipement de protection individuelle

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


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Consulter la Bibliothèque de documents

Didem Seven et al.
Gene, 563(1), 83-86 (2015-03-10)
Different types of genetic and epigenetic changes are associated with HNSCC. The molecular mechanisms of HNSCC carcinogenesis are still undergoing intensive investigation. The Deleted in lung and esophageal cancer 1 (DLEC1) gene is frequently silenced by methylation in various kinds
Patricia Verdier et al.
Methods in molecular biology (Clifton, N.J.), 1454, 15-33 (2016-08-16)
A growing number of studies have used new generation technologies to characterize the protein constituents of cilia and centrosomes. This has led to the identification of a vast number of candidate ciliary or centrosomal proteins, whose subcellular localization needs to
Qian Zhang et al.
The Journal of urology, 184(2), 731-737 (2010-07-20)
Identifying tumor suppressor genes silenced by promoter CpG methylation uncovers mechanisms of tumorigenesis and identifies new epigenetic biomarkers for early cancer detection. DLEC1 is located at 3p22.3, a critical tumor suppressor gene locus for renal cell carcinoma. We explored its
Youwei Zhang et al.
Clinical lung cancer, 11(4), 264-270 (2010-07-16)
Deleted in lung and esophageal cancer 1 (DLEC1) gene was a new candidate tumor suppressor gene. We determined the expression level and methylation status of DLEC1 in non-small-cell lung cancer (NSCLC), and the DLEC1 methylation in plasma DNA as a
Guo-Hua Qiu et al.
Hepatitis monthly, 15(11), e29829-e29829 (2016-02-03)
The molecular mechanisms of tumor suppressor gene DLEC1 are largely unknown. In this study, we established DLEC1 over-expression stable clones to study the cellular function of DLEC1 in the colorectal cancer cell line, HCT116. Stable clones with DLEC1 over-expression were

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