Slc33a1 (GeneName), Acetyl-coenzyme A transporter 1 (ProteinName), ACATN_MOUSE.
Product Name:
Mouse Slc33a1/ Acetyl-coenzyme A transporter 1 ELISA Kit
Cat.#:
-
Brand:
EIAab®
Regulatory Status:
Alternative:
AT-1, Solute carrier family 33 member 1, Acatn
Detection Method:
ELISA
Specificity:
Natural and recombinant mouse Acetyl-coenzyme A transporter 1
Sample Type:
Serum, plasma, tissue homogenates, cell culture supernates and other biological fluids
Sample Data:
Research Area:
-
- Data
- Citations
- Publication
- Sequence / 3D
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General Annotation
Sub Unit:
N/A
Function:
Probable acetyl-CoA transporter necessary for O-acetylation of gangliosides (PubMed:10570973). Negatively regulates BMP signaling.
Subcellular Location:
Endoplasmic reticulum membrane
Multi-pass membrane protein
Database link
This product has not yet been referenced specifically in any publications.
[1].
"A missense mutation in SLC33A1, which encodes the acetyl-CoA transporter, causes autosomal-dominant spastic paraplegia (SPG42)."
[2].
"Expression cloning and characterization of a cDNA encoding a novel membrane protein required for the formation of O-acetylated ganglioside: a putative acetyl-CoA transporter."
[3].
"Identification and functional analysis of a SLC33A1: c.339T>G (p.Ser113Arg) variant in the original SPG42 family."
[4].
"Mutations in SLC33A1 cause a lethal autosomal-recessive disorder with congenital cataracts, hearing loss, and low serum copper and ceruloplasmin."
[5].
"A total of 220 patients with autosomal dominant spastic paraplegia do not display mutations in the SLC33A1 gene (SPG42)."
[7].
"The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC)."
[8].
"Architecture of the human interactome defines protein communities and disease networks."
[9].
"Increased expression of AT-1/SLC33A1 causes an autistic-like phenotype in mice by affecting dendritic branching and spine formation."
[10].
"A human interactome in three quantitative dimensions organized by stoichiometries and abundances."
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