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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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SLC27A4 gene mutation is responsible in the diagnosis of ichthyosis (Montrer LBR Anticorps) 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 (Montrer ATG4B Anticorps) 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.
we resequenced the SLC27A3 (Montrer FATP3 Anticorps) and SLC27A4 genes using 267 autism spectrum disorders(ASD (Montrer ARSD Anticorps)) patient and 1140 control samples and detected 47 and 30 variants for the SLC27A3 (Montrer FATP3 Anticorps) and SLC27A4, revealing that they are highly polymorphic with multiple rare variants.
We describe two siblings with ichthyosis (Montrer LBR Anticorps) 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 (Montrer CD28 Anticorps) CD36 (Montrer CD36 Anticorps)/FAT directly facilitates fatty acid transport across the plasma membrane, whereas the intracellular acyl-CoA (Montrer GNPAT Anticorps) synthetases FATP4 and ACSL1 (Montrer Acsl1 Anticorps) 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 (Montrer LBR Anticorps) prematurity syndrome, a congenital ichthyosis (Montrer LBR Anticorps) caused by FATP4 deficiency. [review]
FATP4, ichthyin (Montrer NIPAL4 Anticorps) and TGM1 (Montrer TGM1 Anticorps) 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
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 (Montrer LBR Anticorps)
A key role was demonstrated for FATP4 in oleic acide-induced GLP-1 (Montrer GCG Anticorps) secretion from the murine intestinal L cell in vitro and in vivo.
even though hypoxia regulates the expression of FATP2 (Montrer SLC27A2 Anticorps) and FATP4 in human trophoblasts, mouse Fatp2 (Montrer SLC27A2 Anticorps) and Fatp4 are not essential for intrauterine fetal growth.
FATP4 contributes as an enzyme to the basal and insulin (Montrer INS Anticorps)-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 (Montrer EGFR Anticorps) and Stat3 (Montrer STAT3 Anticorps) signaling.
Fatp4-null mice displayed features of a neonatally lethal restrictive dermopathy. Lipid analysis demonstrated a disturbed fatty acid composition of epidermal ceramides.
FATP4 exhibits intrinsic acyl-coa synthetase activity and is a high velocity enzyme relative to FATP1.
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