Mouse Anti-BAAT Recombinant Antibody (CBYY-0105) (CBMAB-0105-YY)

Name: Mouse Anti-BAAT Recombinant Antibody (CBYY-0105)
SKU: CBMAB-0105-YY
Rating: 5 (1 reviews)

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Published Data

Mouse Anti-BAAT Recombinant Antibody (CBYY-0105) in Immunoblot

Immunoblot analyses of liver extracts from control mice and mice subjected to sepsis by PCI (a) and quantitation of phospho-Akt (pAkt)/Akt levels normalised to sham control (b). ...View More

Beer, A. J., Hertz, D., Seemann, E., Beretta, M., Westermann, M., Bauer, R., ... & Qualmann, B. (2020). Reduced Mrp2 surface availability as PI3Kγ-mediated hepatocytic dysfunction reflecting a hallmark of cholestasis in sepsis. Scientific Reports, 10(1), 13110.

Datasheet

SDS

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Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Mouse

Clone

CBYY-0105

Application

ELISA, WB, IP

Immunogen

Recombinant BAAT of human origin.

Specificity

Human

Antibody Isotype

IgG1, κ

Clonality

Monoclonal

Application Notes

The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Application	Note
WB	1:100-1:1,000
IP	1-2 µg per 100-500 µg of total protein (1 ml of cell lysate)
ELISA	1:100-1:1,000

Formulations & Storage [For reference only, actual COA shall prevail!]

Format

Liquid

Buffer

PBS, 0.1% gelatin

Preservative

< 0.1% sodium azide

Concentration

0.1 mg/ml

Storage

Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Epitope

N-terminus

More Infomation

Target

Full Name

bile acid Coenzyme A: amino acid N-acyltransferase (glycine N-choloyltransferase)

Introduction

The protein encoded by this gene is a liver enzyme that catalyzes the transfer of C24 bile acids from the acyl-CoA thioester to either glycine or taurine, the second step in the formation of bile acid-amino acid conjugates. The bile acid conjugates then act as a detergent in the gastrointestinal tract, which enhances lipid and fat-soluble vitamin absorption. Defects in this gene are a cause of familial hypercholanemia (FHCA). Two transcript variants encoding the same protein have been found for this gene.

Entrez Gene ID

570

UniProt ID

Q14032

Alternative Names

Bile Acid-CoA:Amino Acid N-Acyltransferase; Bile Acid CoA: Amino Acid N-Acyltransferase (Glycine N-Choloyltransferase); Long-Chain Fatty-Acyl-CoA Hydrolase; Glycine N-Choloyltransferase; BACAT; BAT;

Function

Catalyzes the amidation of bile acids (BAs) with the amino acids taurine and glycine (PubMed:12810727, PubMed:8034703, PubMed:2037576, PubMed:12239217).
More than 95% of the BAs are N-acyl amidates with glycine and taurine (PubMed:8034703).
Amidation of BAs in the liver with glycine or taurine prior to their excretion into bile is an important biochemical event in bile acid metabolism (PubMed:12810727).
This conjugation (or amidation) plays several important biological roles in that it promotes the secretion of BAs and cholesterol into bile and increases the detergent properties of BAs in the intestine, which facilitates lipid and vitamin absorption (PubMed:12810727).
May also act as an acyl-CoA thioesterase that regulates intracellular levels of free fatty acids (PubMed:12810727, PubMed:8034703, PubMed:12239217).
In vitro, catalyzes the hydrolysis of long- and very long-chain saturated acyl-CoAs to the free fatty acid and coenzyme A (CoASH), and conjugates glycine to these acyl-CoAs (PubMed:12810727).

Biological Process

Acyl-CoA metabolic process Source: UniProtKB
Animal organ regeneration Source: Ensembl
Bile acid biosynthetic process Source: UniProtKB
Bile acid conjugation Source: UniProtKB
Bile acid metabolic process Source: Reactome
Fatty acid metabolic process Source: GO_Central
Glycine metabolic process Source: UniProtKB
Liver development Source: Ensembl
Protein localization Source: Reactome
Taurine metabolic process Source: UniProtKB

Cellular Location

Cytosol; Peroxisome

Involvement in disease

Familial hypercholanemia (FHCA): A disorder characterized by elevated serum bile acid concentrations, itching, and fat malabsorption.

Qin, X., Zhang, Y., Lu, J., Huang, S., Liu, Z., & Wang, X. (2021). CYP3A deficiency alters bile acid homeostasis and leads to changes in hepatic susceptibility in rats. Toxicology and Applied Pharmacology, 115703.

Alrehaili, B. D., Lee, M., Takahashi, S., Gonzalez, F. J., & Lee, Y. K. (2020). Mice with Bile acid‐CoA: amino acid N‐acyltransferase deletion are Protected from Obesity. The FASEB Journal, 34(S1), 1-1.

Alonso-Peña, M., Geier, A., & Hermanns, H. (2020). Suppression of bile acid-CoA: amino acid N-acyltransferase gene expression by Oncostatin M. Zeitschrift für Gastroenterologie, 58(01), 3-29.

Civitello, M. L., Denton, R., Zasloff, M. A., & Malone, J. H. (2019). Activation of the Bile Acid Pathway and No Observed Antimicrobial Peptide Sequences in the Skin of a Poison Frog. G3: Genes, Genomes, Genetics, 9(2), 581-589.

Alonso-Pena, M., Geier, A., & Hermanns, H. M. (2019). Suppression of bile acid-CoA: amino acid N-acyltransferase gene expression by the interleukin-6-type cytokine Oncostatin M. Zeitschrift für Gastroenterologie, 57(01), P1-1.

Obuz, U. B., & Lay, I. (2019). Pathways and Inborn Errors of Bile Acid Synthesis. Acta Medica, 50(4), 48-56.

Kirilenko, B. M., Hagey, L. R., Barnes, S., Falany, C. N., & Hiller, M. (2019). Evolutionary analysis of bile acid-conjugating enzymes reveals a complex duplication and reciprocal loss history. Genome biology and evolution, 11(11), 3256-3268.

Nittono, H., Kimura, A., Takei, H., Kurosawa, T., & Iida, T. (2017). Bile Acids and Cholestatic Liver Disease 3: Inborn Errors of Bile Acid Synthesis. In Bile Acids in Gastroenterology (pp. 135-144). Springer, Tokyo.

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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme-Linked Immunospot (ELISpot)
Proteogenomics
Other Protocols

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Isotype control

For research use only. Not intended for any clinical use.

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