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Human Monoclonal SLC27A4 Primary Antibody pour ELISA, WB - ABIN564768
Sandoval, Fraisl, Arias-Barrau, Dirusso, Singer, Sealls, Black: Fatty acid transport and activation and the expression patterns of genes involved in fatty acid trafficking. dans Archives of biochemistry and biophysics 2008
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Cow (Bovine) Polyclonal SLC27A4 Primary Antibody pour WB - ABIN2781620
Xue, Zhao, Wei, Jia: Effect of bromide ion on isolated fractions of dissolved organic matter in secondary effluent during chlorination. dans Journal of hazardous materials 2008
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high SLC27A4 is associated with tumor progression in breast cancer cells.
Case Report: ichthyosis prematurity syndrome caused by novel homozygous mutation in SLC27A4.
SLC27A4 gene mutation is responsible in the diagnosis of ichthyosis prematurity syndrome in a premature infant.
expand the mutational repertory of FATP4 with three undescribed pathogenic mutations in two families
The results have interesting implications that SLC27A4/ATG4B complex might be conducive to the occurrence of autophagy in human cancer cells, which is meaningful investigations toward the aim of developing autophagy-targeting drugs and have significant values in clinical application.
no association between placental expression and maternal body mass index
we resequenced the SLC27A3 and SLC27A4 genes using 267 autism spectrum disorders(ASD) patient and 1140 control samples and detected 47 and 30 variants for the SLC27A3 and SLC27A4, revealing that they are highly polymorphic with multiple rare variants.
We describe two siblings with ichthyosis prematurity syndrome and report a recurrent homozygous mutation (c.1430T>A) that is predicted to lead to a p.Val477Asp substitution in fatty acid transport protein 4.
the cell surface protein CD36/FAT directly facilitates fatty acid transport across the plasma membrane, whereas the intracellular acyl-CoA synthetases FATP4 and ACSL1 enhance fatty acid uptake indirectly by metabolic trapping
the clinical implications of defects in these transporters and relevant animal models, including the FATP4 animal models and ichthyosis prematurity syndrome, a congenital ichthyosis caused by FATP4 deficiency. [review]
FATP4, ichthyin and TGM1 interact in lipid processing essential for maintaining the epidermal barrier function
FATP4 plays crucial roles in the development and maturation of both sebaceous and meibomian glands, as well as in the formation and composition of sebum
FATP1 and FATP4 proteins perform different functional roles in handling long chain fatty acids in skeletal muscle
even though hypoxia regulates the expression of FATP2 and FATP4 in human trophoblasts, mouse Fatp2 and Fatp4 are not essential for intrauterine fetal growth.
Mutation in FATP4 in a patient with self-healing congenital verruciform hyperkeratosis.(
findings propose fatty acid transport protein 4 as a candidate gene for the insulin resistance syndrome
intra-pair correlations revealed that FATP4 expression was significantly up-regulated in acquired obesity."
Data suggest that endogenous FATP4 does not function to translocate fatty acids across the plasma membrane, but functions more as a very long-chain acyl-CoA synthetase.
Mutations in FATP4 gene cause the ichthyosis prematurity syndrome.
The mRNA levels of FATP4 in the placenta in the high-fat diet group were significantly upregulated compared to the control diet group.
Transgenic expression of FATP1 in suprabasal keratinocytes rescued the phenotype of Fatp4 mutants, and FATP1 sorted to the same intracellular organelles as endogenous FATP4
a spontaneous Fatp4/Scl27a4 splice site mutation in congenital ichthyosis
A key role was demonstrated for FATP4 in oleic acide-induced GLP-1 secretion from the murine intestinal L cell in vitro and in vivo.
FATP4 contributes as an enzyme to the basal and insulin-mediated fatty acid uptake of CC muscle cells.
adipocyte-specific Fatp4 deficiency results in adipose hypertrophy and profound alterations in the metabolism of complex lipids.
Epidermal hyperproliferation in mice lacking FATP4 involves ectopic EGF receptor and Stat3 signaling.
identification of critical role in skin and hair development
Fatp4-null mice displayed features of a neonatally lethal restrictive dermopathy. Lipid analysis demonstrated a disturbed fatty acid composition of epidermal ceramides.
role in fat absorption in early embryogenesis and suggests a novel requirement for function during development
FATP4 exhibits intrinsic acyl-coa synthetase activity and is a high velocity enzyme relative to FATP1.
Fatp4 in epidermal keratinocytes is essential for the maintenance of a normal epidermal structure.
FATP4 drives fatty acid uptake indirectly by esterification. It is not a transporter protein involved in fatty acid translocation at the plasma membrane.
in murine skin fibroblasts, FATP4 is the major enzyme producing very long chain fatty acid-CoA for lipid metabolic pathways
Fatp4(-/-);Ivl-Fatp4(tg/+) mice and wild-type littermates displayed indistinguishable food consumption, growth, and weight gain on either low or high fat (Western) diets, with no differences in intestinal triglyceride (TG) absorption or fecal fat losses.
This gene encodes a member of a family of fatty acid transport proteins, which are involved in translocation of long-chain fatty acids cross the plasma membrane. This protein is expressed at high levels on the apical side of mature enterocytes in the small intestine, and appears to be the principal fatty acid transporter in enterocytes. Clinical studies suggest this gene as a candidate gene for the insulin resistance syndrome. Mutations in this gene have been associated with ichthyosis prematurity syndrome.
solute carrier family 27 (fatty acid transporter), member 4
, long-chain fatty acid transport protein 4
, fatty acid transport protein 4
, solute carrier family 27 member 4