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Normal human adipose tissue functions and differentiation has been found in rhabdomyolysis patients with biallelic LPIN1 inactivating mutations.
conclude that Lipin-1 can antagonize HSC (show FUT1 Proteins) activation through the inhibition of TGF-beta (show TGFB1 Proteins)/SMAD (show SMAD1 Proteins) signaling and that resveratrol may affect Lipin-1 gene induction and contribute to the inhibition of TGF-beta (show TGFB1 Proteins)-mediated hepatic fibrogenesis
beta-TRCP depletion in HepG2 hepatocellular carcinoma cells (show BTRC Proteins)resulted in increased Lipin1 protein abundance.
This study showed that LPIN1 knockdown blocks phospholipid synthesis and changes membrane lipid compositions, and that lipin-1 knockdown significantly inhibits tumor growth in vivo using an orthotopic xenograft breast mouse model.
The novel insights into the regulation of human Lipin-1 stability will be useful in planning further studies to elucidate its metabolic processes.
It seems that a new signaling axis, SIRT1 (show SIRT1 Proteins)-SFRS10 (show TRA2B Proteins)-LPIN1 axis, acting in the pathogenesis of alcoholic fatty liver disease exists.
Consistent with these observations, LPIN1 levels were positively correlated with IRS1 (show IRS1 Proteins) expression in human breast cancer. Thus, our results indicate a mechanism by which IRS1 (show IRS1 Proteins) expression is increased in breast cancer, and LPIN1 may be a promising drug target for anticancer therapy
LPIN1 is upregulated in non-alcoholic fatty liver disease. Up-regulation of miR-122 can trigger the compensatory response of LPIN1 and CTDNEP1 in hepatosteatosis.
lipin-1-mediated downregulation of p21 (show CDKN1A Proteins) is critical for the progress of keratinocyte differentiation
lipin-1 has a critical role in the regulation of macrophage inflammatory responses to modified-LDL
Study demonstrated that chronic alcohol feeding resulted in adipose tissue lipodystrophy and subsequent liver injury including ER stress and apoptosis. Overexpression of LPIN1 in adipose tissue protected mice against alcohol-induced liver injury through restoration of WAT lipid storage function and leptin secretion suggesting that LPIN1 plays a significant role in the pathogenesis of alcohol-induced lipodystrophy and ALD.
Suppression of lipin 1 and lipin2 (show LPIN2 Proteins) are the primary mechanism of increased phosphatidic acid levels in the liver during acetaminophen-induced liver injury and recovery.
Data demonstrate that myeloid cell-specific deletion of lipin-1 ameliorated inflammation and alcoholic hepatitis in mice via activation of endocrine adiponectin-FGF15 signaling.
Data suggest that phosphorylation does not affect catalytic activity of lipin 3 (show LPIN3 Proteins) or its ability to associate with phosphatidic acid in vitro; different polybasic domains in lipin 1 and lipin 3 (show LPIN3 Proteins) are responsible for phospho-regulation on the former but not the latter enzyme.
Data indicate a critical physiological function of beta-TRCP (show BTRC Proteins) in regulating hepatic lipid metabolic homeostasis in part through modulating Lipin1 stability.
The insulin resistance induced by lipin-1 downregulation was related to the disturbance of lipid homeostasis. Lipin-1 silencing reduced intracellular DAG and TAG levels, but elevated ceramide accumulation in C2C12 myotubes
Time course analysis demonstrated that the adipogenic 'hub', sampled by PPARgamma (show PPARG Proteins) and Lpin1, undergoes orchestrated reorganization during adipogenesis.
Our findings provide new insights into the physiological roles of hepatic Lipin1 in systemic energy homeostasis, and suggest that the moderate inactivation of hepatic Lipin1 represents a promising approach for preventing the development of obesity.
c-fos has a role in increasing the catalytic efficiency of lipin 1 beta
The lipin1 gene may have a crucial effect on body lipid accumulation in pigs.
Different genotypes of the Lpin1 gene were associated with percentage of leaf fat and intramuscular fat.
The results of this study suggest that suggest that SLC27A6, ACSL1 (show Acsl1 Proteins), FABP3 (show FABP3 Proteins), AGPAT6 (show AGPAT6 Proteins), and LPIN1 coordinately regulate the channeling of fatty acids toward copious milk fat synthesis in bovine mammary.
This gene encodes a magnesium-ion-dependent phosphatidic acid phosphohydrolase enzyme that catalyzes the penultimate step in triglyceride synthesis including the dephosphorylation of phosphatidic acid to yield diacylglycerol. Expression of this gene is required for adipocyte differentiation and it also functions as a nuclear transcriptional coactivator with some peroxisome proliferator-activated receptors to modulate expression of other genes involved in lipid metabolism. Mutations in this gene are associated with metabolic syndrome, type 2 diabetes, and autosomal recessive acute recurrent myoglobinuria (ARARM). This gene is also a candidate for several human lipodystrophy syndromes. Alternative splicing results in multiple transcript variants encoding distinct isoforms. Additional splice variants have been described but their full-length structures have not been determined.
, phosphatidate phosphatase LPIN1-like
, phosphatidate phosphatase LPIN1
, fatty liver dystrophy protein