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Members of the perilipin family, such as PLIN5, coat intracellular lipid storage droplets and protect them from lipolytic degradation (Dalen et al., 2007 [PubMed 17234449]).[supplied by OMIM, Feb 2010].. 再加上，我们可以发Perilipin 5 试剂盒 (5) 和 Perilipin 5 蛋白 (5)和数多这个蛋白质的别的产品。
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Cow (Bovine) Polyclonal PLIN5 Primary Antibody for IHC, IHC (fro) - ABIN258761
Revuelta-López, Cal, Julve, Rull, Martínez-Bujidos, Perez-Cuellar, Ordoñez-Llanos, Badimon, Sanchez-Quesada, Llorente-Cortés: Hypoxia worsens the impact of intracellular triglyceride accumulation promoted by electronegative low-density lipoprotein in cardiomyocytes by impairing perilipin 5 upregulation. in The international journal of biochemistry & cell biology 2015
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Human Polyclonal PLIN5 Primary Antibody for SimWes, WB - ABIN258765
Wolins, Quaynor, Skinner, Tzekov, Croce, Gropler, Varma, Yao-Borengasser, Rasouli, Kern, Finck, Bickel: OXPAT/PAT-1 is a PPAR-induced lipid droplet protein that promotes fatty acid utilization. in Diabetes 2006
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C/EBPalpha (显示 CEBPA 抗体) is an essential regulatory factor for perilipin5 transcription and suggest that fasting stimulates perilipin5 transcription through influencing C/EBPalpha (显示 CEBPA 抗体) expression.
The data highlight a key role of PLIN5 in lipid droplets function, first by finely adjusting lipid droplets fatty acids supply to mitochondrial oxidation, and second acting as a protective factor against lipotoxicity in skeletal muscle.
Notch1 expression is reduced and glu (显示 G6PC 抗体)cose-6-phosphatase and (显示 G6PC 抗体) perilipin-5 (G6PC/PLIN5) are upr (显示 NOTCH1 抗体)egulated in liver biopsies from nonalcoholic steatohepatitis (NASH) and nonalcoholic fatty liver disease (NAFLD) patients.
High oxygen consumption in middle-aged men was reflected in higher perilipin 5 expression in skeletal muscle.
PLIN5 was significantly colocated with ATGL (显示 PNPLA2 抗体), mitochondria and CGI-58 (显示 ABHD5 抗体), indicating a close association between the key lipolytic effectors in resting skeletal muscle.
Perilipin 5 as a lipid droplet protein adapted to mitochondrial energy utilization
Sprint interval and traditional endurance training increase net intramuscular triglyceride breakdown and expression of perilipin 2 (显示 PLIN2 抗体) and 5
PLIN5 likely plays an important role in intramyocellular lipid accumulation and oxidation, both of which increase with endurance training in human skeletal muscle.
The lipid droplet coat protein (显示 GOLPH3 抗体) perilipin 5 also localizes to muscle mitochondria.
Perilipin 5 is the most recently established family member, highly expressed in oxidative tissues and could play an important role in regulating LD TAG hydrolysis in oxidative mammalian tissues. [Review]
interaction of ATGL (显示 PNPLA2 抗体) with CGI-58 (显示 ABHD5 抗体) increased lipolysis, whereas interaction of ATGL (显示 PNPLA2 抗体) with perilipin 5 decreased lipolysis.
Plin5, a new regulator of myocardial lipid metabolism, decreases free fatty acid peroxidation by inhibiting the lipolysis of intracellular lipid droplets, thus providing cardioprotection against I/R injury and shedding new light on therapeutic solutions for I/R diseases.
During catecholamine-stimulated lipolysis, Perilipin 5 is phosphorylated by protein kinase A and forms transcriptional complexes with PGC-1alpha and SIRT1 (显示 SIRT1 抗体) in the nucleus. Perilipin 5 promotes PGC-1alpha co-activator function by disinhibiting SIRT1 (显示 SIRT1 抗体) deacetylase activity.
Changes in lipid metabolism resulting from PLIN5 deletion reduce ER stress in muscle, decrease FGF21 (显示 FGF21 抗体) production by muscle and liver, and impair glycemic control.
The results indicated that atorvastatin promoted lipolysis and reduced TG accumulation in the liver by increasing PKA-mediated phosphorylation of Plin5. This new mechanism of lipid-lowering effects of atorvastatin might provide a new strategy for NAFLD (显示 TSC2 抗体) treatment.
mitochondria isolated from hearts deficient in Plin5, have specific functional defects
Plin5 deficiency alters cardiac lipid metabolism and associates with reduced survival following myocardial ischemia.
Data show that glucose-6-phosphatase (显示 G6PC 抗体) and perilipin-5 (G6PC (显示 G6PC 抗体)/PLIN5) are upregulated in notch1 (显示 NOTCH1 抗体) knockout (KO) mice.
PLIN5 is dispensable for normal substrate metabolism during exercise and is not required to promote mitochondrial biogenesis or enhance the cellular adaptations to endurance exercise training.
High fat diet-induced liver fibrosis is accompanied by an approximate 75% reduction in Plin5 in hepatic stellate cells (HSC (显示 FUT1 抗体)), and spontaneous activation of primary HSC (显示 FUT1 抗体) produces temporally coincident loss of Plin5 expression and lipid droplet depletion.
Members of the perilipin family, such as PLIN5, coat intracellular lipid storage droplets and protect them from lipolytic degradation (Dalen et al., 2007
lipid storage droplet protein 5
, perilipin 5
, lipid droplet associated protein
, lipid droplet-associated protein PAT-1
, myocardial LD protein