Overview

  • Product nameAnti-ABCB4 antibody
    See all ABCB4 primary antibodies
  • Description
    Goat polyclonal to ABCB4
  • Tested applicationsSuitable for: IHC-Pmore details
  • Species reactivity
    Reacts with: Human
  • Immunogen

    Synthetic peptide, conjugated to KLH corresponding to residues in the N terminal of Human ABCB4.

  • Positive control
    • Human Liver tissue

Properties

Associated products

Applications

Our Abpromise guarantee covers the use of ab111209 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
IHC-P Use a concentration of 3.75 µg/ml. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.

Target

  • FunctionMediates ATP-dependent export of organic anions and drugs from the cytoplasm. Hydrolyzes ATP with low efficiency. Human MDR3 is not capable of conferring drug resistance. Mediates the translocation of phosphatidylcholine across the canalicular membrane of the hepatocyte.
  • Involvement in diseaseDefects in ABCB4 are the cause of progressive familial intrahepatic cholestasis type 3 (PFIC3) [MIM:602347]. PFIC3 is an autosomal recessive liver disorder presenting with early onset cholestasis that progresses to cirrhosis and liver failure before adulthood. It is characterized by elevated serum gamma-glutamyltransferase levels.
    Defects in ABCB4 are a cause of intrahepatic cholestasis of pregnancy (ICP) [MIM:147480]; also known as obstetric cholestasis. ICP is a multifactorial liver disorder of pregnancy. It presents during the second or, more commonly, the third trimestre of pregnancy with intense pruritus which becomes more severe with advancing gestation and cholestasis. Cholestasis results from abnormal biliary transport from the liver into the small intestine. ICP causes fetal distress, spontaneous premature delivery and intrauterine death. ICP patients have spontaneous and progressive disappearance of cholestasis after delivery.
    Defects in ABCB4 are a cause of gallbladder disease type 1 (GBD1) [MIM:600803]. It is one of the major digestive diseases. Gallstones composed of cholesterol (cholelithiasis) are the common manifestations in western countries. Most people with gallstones, however, remain asymptomatic through their lifetimes.
  • Sequence similaritiesBelongs to the ABC transporter superfamily. ABCB family. Multidrug resistance exporter (TC 3.A.1.201) subfamily.
    Contains 2 ABC transmembrane type-1 domains.
    Contains 2 ABC transporter domains.
  • Cellular localizationCell membrane.
  • Information by UniProt
  • Database links
  • Alternative names
    • ABC 21 antibody
    • ABC B4 antibody
    • ABC21 antibody
    • ABCB 4 antibody
    • Abcb4 antibody
    • ABCB4 protein antibody
    • ATP binding cassette sub family B MDR/TAP member 4 antibody
    • ATP binding cassette sub family B member 4 antibody
    • ATP-binding cassette sub-family B member 4 antibody
    • MDR 3 antibody
    • MDR2 antibody
    • MDR2/3 antibody
    • MDR3 antibody
    • MDR3 P glycoprotein antibody
    • MDR3 P gp antibody
    • MDR3_HUMAN antibody
    • Multidrug resistance protein 3 antibody
    • Multiple drug resistance 3 antibody
    • P glycoprotein 3 antibody
    • P-glycoprotein 3 antibody
    • PFIC 3 antibody
    • PFIC3 antibody
    • PGY 3 antibody
    • PGY3 antibody
    see all

Anti-ABCB4 antibody images

  • ab111209, at 3.75 µg/ml, staining ABCB4 in formalin fixed, paraffin embedded Human liver tissue by Immunohistochemistry, followed by biotinylated secondary antibody, alkaline phosphatase streptavidin and chromogen.

References for Anti-ABCB4 antibody (ab111209)

This product has been referenced in:

See 1 Publication for this product

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Thank you for contacting us. ab3364; anti P Glycoprotein is no longer available in our catalogue. However we have similar products available to buy. The catalogue numbers are ab3083; ab3366; ab10333; ab80594; ab80626. Please check the da...

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