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Disease on EC 2.3.1.51 - 1-acylglycerol-3-phosphate O-acyltransferase

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DISEASE
TITLE OF PUBLICATION
LINK TO PUBMED
1-acylglycerol-3-phosphate o-acyltransferase deficiency
ABHD5 blunts the sensitivity of colorectal cancer to fluorouracil via promoting autophagic uracil yield.
ABHD5 interacts with BECN1 to regulate autophagy and tumorigenesis of colon cancer independent of PNPLA2.
Absence of AGPAT2 impairs brown adipogenesis, increases IFN stimulated gene expression and alters mitochondrial morphology.
AGPAT2 deficiency impairs adipogenic differentiation in primary cultured preadipocytes in a non-autophagy or apoptosis dependent mechanism.
Cancer-derived exosomal TRIM59 regulates macrophage NLRP3 inflammasome activation to promote lung cancer progression.
Inherited lipodystrophies and hypertriglyceridemia.
Loss of abhd5 promotes colorectal tumor development and progression by inducing aerobic glycolysis and epithelial-mesenchymal transition.
Macrophage ABHD5 suppresses NF-?B-dependent matrix metalloproteinase expression and cancer metastasis.
Molecular mechanisms of hepatic steatosis and insulin resistance in the AGPAT2-deficient mouse model of congenital generalized lipodystrophy.
Pathology of Congenital Generalized Lipodystrophy in Agpat2 -/-Mice.
Truncation of CGI-58 protein causes malformation of lamellar granules resulting in ichthyosis in Dorfman-Chanarin syndrome.
Adenomatous Polyps
Loss of abhd5 promotes colorectal tumor development and progression by inducing aerobic glycolysis and epithelial-mesenchymal transition.
Carcinogenesis
ABHD5 interacts with BECN1 to regulate autophagy and tumorigenesis of colon cancer independent of PNPLA2.
Loss of abhd5 promotes colorectal tumor development and progression by inducing aerobic glycolysis and epithelial-mesenchymal transition.
Carcinoma
Expression of lysophosphatidic acid acyltransferase beta (LPAAT-beta) in ovarian carcinoma: correlation with tumour grading and prognosis.
Interaction of lipopolysaccharide with a mammalian lyso-phosphatidate acyltransferase (LPAAT) transfected into E. coli, and effect of lisofylline on LPAAT transfected into mammalian cells.
Lipid synthesis and processing proteins ABHD5, PGRMC1 and squalene synthase can serve as novel immunohistochemical markers for sebaceous neoplasms and differentiate sebaceous carcinoma from sebaceoma and basal cell carcinoma with clear cell features.
Lysophosphatidic acid acyltransferase-beta (LPAAT-beta) is highly expressed in advanced ovarian cancer and is associated with aggressive histology and poor survival.
Carcinoma, Basal Cell
Lipid synthesis and processing proteins ABHD5, PGRMC1 and squalene synthase can serve as novel immunohistochemical markers for sebaceous neoplasms and differentiate sebaceous carcinoma from sebaceoma and basal cell carcinoma with clear cell features.
Cardiomyopathies
Inborn errors of cytoplasmic triglyceride metabolism.
Cardiovascular Diseases
Leu124Serfs*26, a novel AGPAT2 mutation in congenital generalized lipodystrophy with early cardiovascular complications.
carnitine o-palmitoyltransferase deficiency
High frequency of ETFDH c.250G>A mutation in Taiwanese patients with late-onset lipid storage myopathy.
Colonic Neoplasms
ABHD5 interacts with BECN1 to regulate autophagy and tumorigenesis of colon cancer independent of PNPLA2.
ColoLipidGene: signature of lipid metabolism-related genes to predict prognosis in stage-II colon cancer patients.
Loss of abhd5 promotes colorectal tumor development and progression by inducing aerobic glycolysis and epithelial-mesenchymal transition.
Colorectal Neoplasms
ABHD5 blunts the sensitivity of colorectal cancer to fluorouracil via promoting autophagic uracil yield.
ABHD5 interacts with BECN1 to regulate autophagy and tumorigenesis of colon cancer independent of PNPLA2.
Enzymatic activity of the human 1-acylglycerol-3-phosphate-O-acyltransferase isoform 11 (AGPAT11): upregulated in breast and cervical cancers.
Loss of abhd5 promotes colorectal tumor development and progression by inducing aerobic glycolysis and epithelial-mesenchymal transition.
Loss of Abhd5 Promotes Colorectal Tumor Development and Progression by Inducing Aerobic Glycolysis and Epithelial-Mesenchymal Transition.
Macrophage ABHD5 promotes colorectal cancer growth by suppressing spermidine production by SRM.
Macrophage ABHD5 suppresses NF-?B-dependent matrix metalloproteinase expression and cancer metastasis.
Coronary Artery Disease
Genome-Wide Association Study Identifies Novel Loci Associated with Circulating Phospho- and Sphingolipid Concentrations.
Dermatitis, Exfoliative
Chanarin Dorfman syndrome: a case report with novel nonsense mutation.
Early onset of Chanarin-Dorfman syndrome with severe liver involvement in a patient with a complex rearrangement of ABHD5 promoter.
Diabetes Mellitus
Leptin ameliorates insulin resistance and hepatic steatosis in Agpat2-/- lipodystrophic mice independent of hepatocyte leptin receptors.
Diabetes Mellitus, Type 2
Genome-Wide Association Study Identifies Novel Loci Associated with Circulating Phospho- and Sphingolipid Concentrations.
Diabetes, Gestational
Downregulated ABHD5 Aggravates Insulin Resistance of Trophoblast Cells During Gestational Diabetes Mellitus.
Dyslipidemias
Inherited non-alcoholic fatty liver disease and dyslipidemia due to monoallelic ABHD5 mutations.
Embryo Loss
Plastid lysophosphatidyl acyltransferase is essential for embryo development in Arabidopsis.
Endometrial Neoplasms
Lysophosphatidic acid acyltransferase-beta is a prognostic marker and therapeutic target in gynecologic malignancies.
Oncogenic role of ABHD5 in endometrial cancer.
Exfoliation Syndrome
Molecular Genetics of Glaucoma: Subtype and Ethnicity Considerations.
NEW GENETIC MARKERS ASSOCIATED WITH SUSCEPTIBILITY TO EXFOLIATION SYNDROME AMONG GEORGIAN POPULATION.
Fatty Liver
Dynamic interactions of ABHD5 with PNPLA3 regulate triacylglycerol metabolism in brown adipocytes.
Early onset of Chanarin-Dorfman syndrome with severe liver involvement in a patient with a complex rearrangement of ABHD5 promoter.
Inherited non-alcoholic fatty liver disease and dyslipidemia due to monoallelic ABHD5 mutations.
Steatohepatitis and unsuspected micronodular cirrhosis in Dorfman-Chanarin syndrome with documented ABHD5 mutation.
Two cases of non-alcoholic fatty liver disease caused by biallelic ABHD5 mutations.
Genetic Diseases, Inborn
Genetics of Exfoliation Syndrome.
Neutral lipid storage disease: genetic disorders caused by mutations in adipose triglyceride lipase/PNPLA2 or CGI-58/ABHD5.
Glucose Metabolism Disorders
Downregulated ABHD5 Aggravates Insulin Resistance of Trophoblast Cells During Gestational Diabetes Mellitus.
Heart Failure
The lipid droplet-associated protein ABHD5 protects the heart through proteolysis of HDAC4.
Hematologic Neoplasms
[Relationship between Lysophosphatide Acid Acyltransferase beta and Tumor - Review.]
Hepatitis C
The ATGL lipase cooperates with ABHD5 to mobilize lipids for hepatitis C virus assembly.
Hepatomegaly
Early onset of Chanarin-Dorfman syndrome with severe liver involvement in a patient with a complex rearrangement of ABHD5 promoter.
The gene encoding adipose triglyceride lipase (PNPLA2) is mutated in neutral lipid storage disease with myopathy.
Hyperlipidemias
A novel mutation of ABHD5 gene in a Chanarin Dorfman patient with unusual dermatological findings.
Hypertriglyceridemia
Inborn errors of cytoplasmic triglyceride metabolism.
Ichthyosiform Erythroderma, Congenital
Early onset of Chanarin-Dorfman syndrome with severe liver involvement in a patient with a complex rearrangement of ABHD5 promoter.
Ichthyosis
ABHD5 stimulates PNPLA1-mediated ?-O-acylceramide biosynthesis essential for a functional skin permeability barrier.
Clinical and genetic analysis of lipid storage myopathies.
High frequency of ETFDH c.250G>A mutation in Taiwanese patients with late-onset lipid storage myopathy.
Inborn errors of cytoplasmic triglyceride metabolism.
Molecular mechanism of the ichthyosis pathology of Chanarin-Dorfman syndrome: Stimulation of PNPLA1-catalyzed ?-O-acylceramide production by ABHD5.
Recurrent N209* ABHD5 mutation in two unreported families with Chanarin Dorfman Syndrome.
Steatohepatitis and unsuspected micronodular cirrhosis in Dorfman-Chanarin syndrome with documented ABHD5 mutation.
The gene encoding adipose triglyceride lipase (PNPLA2) is mutated in neutral lipid storage disease with myopathy.
Truncation of CGI-58 protein causes malformation of lamellar granules resulting in ichthyosis in Dorfman-Chanarin syndrome.
[Neutral lipid storage diseases and ATGL (adipose triglyceride lipase) and CGI-58/ABHD5 (alpha-beta hydrolase domain-containing 5) deficiency: myopathy, ichthyosis, but no obesity]
Infections
Dengue virus reduces AGPAT1 expression to alter phospholipids and enhance infection in Aedes aegypti.
Insulin Resistance
AGPAT2 deficiency impairs adipogenic differentiation in primary cultured preadipocytes in a non-autophagy or apoptosis dependent mechanism.
AGPAT2 gene mutation in a child with Berardinelli-Seip congenital lipodystrophy syndrome.
Alterations in Lipid Signaling Underlie Lipodystrophy Secondary to AGPAT2 Mutations.
Diseases of adipose tissue: genetic and acquired lipodystrophies.
Downregulated ABHD5 Aggravates Insulin Resistance of Trophoblast Cells During Gestational Diabetes Mellitus.
Hepatic gluconeogenesis is enhanced by phosphatidic acid which remains uninhibited by insulin in lipodystrophic Agpat2-/- mice.
How to diagnose a lipodystrophy syndrome.
Human AGPAT isoforms 1 and 2: Biochemical characterization and their inability to rescue hepatic steatosis in Agpat2-/- lipodystrophic mice.
Leptin ameliorates insulin resistance and hepatic steatosis in Agpat2-/- lipodystrophic mice independent of hepatocyte leptin receptors.
Monogenic forms of insulin resistance: apertures that expose the common metabolic syndrome.
[Monogenic severe insulin resistance syndromes]
Intellectual Disability
Dorfman-Chanarin syndrome without mental retardation caused by a homozygous ABHD5 splice site mutation that skips exon 6.
Mutations in Gng3lg and AGPAT2 in Berardinelli-Seip congenital lipodystrophy and Brunzell syndrome: phenotype variability suggests important modifier effects.
Leukemia
Antileukemic activity of lysophosphatidic acid acyltransferase-beta inhibitor CT32228 in chronic myelogenous leukemia sensitive and resistant to imatinib.
Effect of lysophosphatidic acid acyltransferase-beta inhibition in acute leukemia.
[Lysophosphatidic acid acyltransferase ? gene expression in newly diagnosed leukemia patients].
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Antileukemic activity of lysophosphatidic acid acyltransferase-beta inhibitor CT32228 in chronic myelogenous leukemia sensitive and resistant to imatinib.
[Lysophosphatidic acid acyltransferase ? gene expression in newly diagnosed leukemia patients].
Leukemia, Myeloid, Acute
[Lysophosphatidic acid acyltransferase ? gene expression in newly diagnosed leukemia patients].
Leukemia, Promyelocytic, Acute
[Lysophosphatidic acid acyltransferase ? gene expression in newly diagnosed leukemia patients].
Lipodystrophy
A Frame-Shift Mutation in CAV1 Is Associated with a Severe Neonatal Progeroid and Lipodystrophy Syndrome.
A regulatory role for 1-acylglycerol-3-phosphate-O-acyltransferase 2 in adipocyte differentiation.
A Single Complex Agpat2 Allele in a Patient With Partial Lipodystrophy.
AGPAT2 deficiency impairs adipogenic differentiation in primary cultured preadipocytes in a non-autophagy or apoptosis dependent mechanism.
AGPAT2 gene mutation in a child with Berardinelli-Seip congenital lipodystrophy syndrome.
AGPAT2 is essential for postnatal development and maintenance of white and brown adipose tissue.
Alterations in Lipid Signaling Underlie Lipodystrophy Secondary to AGPAT2 Mutations.
Case report: Dental management of Berardinelli-Seip congenital lipodystrophy.
Congenital generalized lipodystrophy: significance of triglyceride biosynthetic pathways.
Discovering metabolic disease gene interactions by correlated effects on cellular morphology.
Early infantile cardiomyopathy and liver disease: a multisystemic disorder caused by congenital lipodystrophy.
Efficacy of leptin therapy in the different forms of human lipodystrophy.
Erratum to: Identification and Characterisation of a Novel Pathogenic Mutation in the Human Lipodystrophy Gene AGPAT2 : C48R: A Novel Mutation in AGPAT2.
Exploring the pathophysiology behind the more common genetic and acquired lipodystrophies.
Genetic basis of congenital generalized lipodystrophy.
Genetic disorders of adipose tissue development, differentiation, and death.
Higher adiponectin levels in patients with Berardinelli-Seip congenital lipodystrophy due to seipin as compared with 1-acylglycerol-3-phosphate-o-acyltransferase-2 deficiency.
Identification and Characterisation of a Novel Pathogenic Mutation in the Human Lipodystrophy Gene AGPAT2 : C48R: A Novel Mutation in AGPAT2.
Inherited lipodystrophies and hypertriglyceridemia.
Lipodystrophies: Disorders of adipose tissue biology.
Monogenic forms of insulin resistance: apertures that expose the common metabolic syndrome.
Mutations in Gng3lg and AGPAT2 in Berardinelli-Seip congenital lipodystrophy and Brunzell syndrome: phenotype variability suggests important modifier effects.
Mutations in the seipin and AGPAT2 genes clustering in consanguineous families with Berardinelli-Seip congenital lipodystrophy from two separate geographical regions of Brazil.
Novel BSCL2 gene mutation E189X in Chinese congenital generalized lipodystrophy child with early onset diabetes mellitus.
Oligomers of the lipodystrophy protein seipin may co-ordinate GPAT3 and AGPAT2 enzymes to facilitate adipocyte differentiation.
Pathology of Congenital Generalized Lipodystrophy in Agpat2 -/-Mice.
Phenotypic and genetic heterogeneity in congenital generalized lipodystrophy.
Phenotypic heterogeneity in biochemical parameters correlates with mutations in AGPAT2 or Seipin genes among Berardinelli-Seip congenital lipodystrophy patients.
Prevalence of mutations in AGPAT2 among human lipodystrophies.
Lipodystrophy, Congenital Generalized
A novel AGPAT2 mutation associated with a case of late-diagnosed congenital generalized lipodystrophy type 1.
A Patient with Congenital Generalized Lipodystrophy Due To a Novel Mutation in BSCL2: Indications for Secondary Mitochondrial Dysfunction.
A rare frameshift mutation in the AGPAT2 gene in a family from gaza with congenital generalized lipodystrophy.
A regulatory role for 1-acylglycerol-3-phosphate-O-acyltransferase 2 in adipocyte differentiation.
A Single Complex Agpat2 Allele in a Patient With Partial Lipodystrophy.
Absence of AGPAT2 impairs brown adipogenesis, increases IFN stimulated gene expression and alters mitochondrial morphology.
AGPAT2 gene mutation in a child with Berardinelli-Seip congenital lipodystrophy syndrome.
AGPAT2 is mutated in congenital generalized lipodystrophy linked to chromosome 9q34.
Alterations in Lipid Signaling Underlie Lipodystrophy Secondary to AGPAT2 Mutations.
Berardinelli-Seip syndrome patient with novel AGPAT2 splicesite mutation and concomitant development of non-diabetic polyneuropathy
Case report: Dental management of Berardinelli-Seip congenital lipodystrophy.
Description of an AGPAT2 pathologic allelic variant in a 54-year-old Caucasian woman with Berardinelli-Seip syndrome.
Diseases of adipose tissue: genetic and acquired lipodystrophies.
Divergent metabolic phenotype between two sisters with congenital generalized lipodystrophy due to double AGPAT2 homozygous mutations. a clinical, genetic and in silico study.
Enzymatic activity of naturally occurring 1-acylglycerol-3-phosphate-O-acyltransferase 2 mutants associated with congenital generalized lipodystrophy.
Exploring the pathophysiology behind the more common genetic and acquired lipodystrophies.
Expression of AGPAT2, an enzyme involved in the glycerophospholipid/triacylglycerol biosynthesis pathway, is directly regulated by HIF-1 and promotes survival and etoposide resistance of cancer cells under hypoxia.
Further delineation of AGPAT2 and BSCL2 related congenital generalized lipodystrophy in young infants.
Genetic basis of congenital generalized lipodystrophy.
Identification of a novel nonsense mutation and a missense substitution in the AGPAT2 gene causing congenital generalized lipodystrophy type 1.
Inherited lipodystrophies and hypertriglyceridemia.
Leptin ameliorates insulin resistance and hepatic steatosis in Agpat2-/- lipodystrophic mice independent of hepatocyte leptin receptors.
Leu124Serfs*26, a novel AGPAT2 mutation in congenital generalized lipodystrophy with early cardiovascular complications.
Lipodystrophies: Disorders of adipose tissue biology.
Lipodystrophies: Genetic and Acquired Body Fat Disorders.
Metabolic, Reproductive, and Neurologic Abnormalities in Agpat1-Null Mice.
Molecular mechanisms of hepatic steatosis and insulin resistance in the AGPAT2-deficient mouse model of congenital generalized lipodystrophy.
Monogenic forms of insulin resistance: apertures that expose the common metabolic syndrome.
Mutations in Gng3lg and AGPAT2 in Berardinelli-Seip congenital lipodystrophy and Brunzell syndrome: phenotype variability suggests important modifier effects.
Mutations in the seipin and AGPAT2 genes clustering in consanguineous families with Berardinelli-Seip congenital lipodystrophy from two separate geographical regions of Brazil.
Novel BSCL2 gene mutation E189X in Chinese congenital generalized lipodystrophy child with early onset diabetes mellitus.
Novel mutations of the BSCL2 and AGPAT2 genes in ten families with Berardinelli-Seip congenital generalized lipodystrophy syndrome.
Oil Red-O Positive lipid blobs on peripheral blood film examination in a muscular infant with the diagnosis of Berardinelli-Seip syndrome.
Pathology of Congenital Generalized Lipodystrophy in Agpat2 -/-Mice.
Phenotypic and genetic heterogeneity in congenital generalized lipodystrophy.
Phenotypic heterogeneity in biochemical parameters correlates with mutations in AGPAT2 or Seipin genes among Berardinelli-Seip congenital lipodystrophy patients.
Phenotypic heterogeneity in body fat distribution in patients with congenital generalized lipodystrophy caused by mutations in the AGPAT2 or seipin genes.
Seipin oligomers can interact directly with AGPAT2 and lipin 1, physically scaffolding critical regulators of adipogenesis.
[Identification of a novel AGPAT2 variant in a Chinese patient with congenital generalized lipodystrophy type 1].
[Primary lipodystrophies]
Lipodystrophy, Familial Partial
Monogenic forms of insulin resistance: apertures that expose the common metabolic syndrome.
Liver Cirrhosis
Liver cirrhosis in an infant with Chanarin-Dorfman syndrome caused by a novel splice-site mutation in ABHD5.
Liver Diseases
Dynamic interactions of ABHD5 with PNPLA3 regulate triacylglycerol metabolism in brown adipocytes.
Inherited non-alcoholic fatty liver disease and dyslipidemia due to monoallelic ABHD5 mutations.
Two cases of non-alcoholic fatty liver disease caused by biallelic ABHD5 mutations.
Lung Neoplasms
Cancer-derived exosomal TRIM59 regulates macrophage NLRP3 inflammasome activation to promote lung cancer progression.
Lymphatic Metastasis
Oncogenic role of ABHD5 in endometrial cancer.
Lymphoma
Induction of apoptosis using inhibitors of lysophosphatidic acid acyltransferase-beta and anti-CD20 monoclonal antibodies for treatment of human non-Hodgkin's lymphomas.
Lymphoma, Non-Hodgkin
Induction of apoptosis using inhibitors of lysophosphatidic acid acyltransferase-beta and anti-CD20 monoclonal antibodies for treatment of human non-Hodgkin's lymphomas.
Marfan Syndrome
How to diagnose a lipodystrophy syndrome.
Metabolic Syndrome
Monogenic forms of insulin resistance: apertures that expose the common metabolic syndrome.
Multiple Myeloma
Antitumor activity of lysophosphatidic acid acyltransferase-beta inhibitors, a novel class of agents, in multiple myeloma.
Muscular Diseases
Clinical and genetic analysis of lipid storage myopathies.
High frequency of ETFDH c.250G>A mutation in Taiwanese patients with late-onset lipid storage myopathy.
Inborn errors of cytoplasmic triglyceride metabolism.
The gene encoding adipose triglyceride lipase (PNPLA2) is mutated in neutral lipid storage disease with myopathy.
[Neutral lipid storage diseases and ATGL (adipose triglyceride lipase) and CGI-58/ABHD5 (alpha-beta hydrolase domain-containing 5) deficiency: myopathy, ichthyosis, but no obesity]
Neoplasm Metastasis
Lysophosphatidic acid acyltransferase-beta (LPAAT-beta) is highly expressed in advanced ovarian cancer and is associated with aggressive histology and poor survival.
Macrophage ABHD5 suppresses NF-?B-dependent matrix metalloproteinase expression and cancer metastasis.
Oncogenic role of ABHD5 in endometrial cancer.
Neoplasms
ABHD5 interacts with BECN1 to regulate autophagy and tumorigenesis of colon cancer independent of PNPLA2.
ABHD5 suppresses cancer cell anabolism through lipolysis-dependent activation of the AMPK/mTORC1 pathway.
Antileukemic activity of lysophosphatidic acid acyltransferase-beta inhibitor CT32228 in chronic myelogenous leukemia sensitive and resistant to imatinib.
Cancer-derived exosomal TRIM59 regulates macrophage NLRP3 inflammasome activation to promote lung cancer progression.
Circular RNA cMras Suppresses the Progression of Lung Adenocarcinoma Through ABHD5/ATGL Axis Using NF-?B Signaling Pathway.
Cloning and expression of two human lysophosphatidic acid acyltransferase cDNAs that enhance cytokine-induced signaling responses in cells.
Effect of lysophosphatidic acid acyltransferase-beta inhibition in acute leukemia.
Enzymatic activity of the human 1-acylglycerol-3-phosphate-O-acyltransferase isoform 11 (AGPAT11): upregulated in breast and cervical cancers.
Expression of AGPAT2, an enzyme involved in the glycerophospholipid/triacylglycerol biosynthesis pathway, is directly regulated by HIF-1 and promotes survival and etoposide resistance of cancer cells under hypoxia.
Expression of lysophosphatidic acid acyltransferase beta (LPAAT-beta) in ovarian carcinoma: correlation with tumour grading and prognosis.
Identification of a Novel Human Lysophosphatidic Acid Acyltransferase, LPAAT-theta, Which Activates mTOR Pathway.
Inhibition of lysophosphatidic acid acyltransferase beta disrupts proliferative and survival signals in normal cells and induces apoptosis of tumor cells.
Lipid synthesis and processing proteins ABHD5, PGRMC1 and squalene synthase can serve as novel immunohistochemical markers for sebaceous neoplasms and differentiate sebaceous carcinoma from sebaceoma and basal cell carcinoma with clear cell features.
Loss of abhd5 promotes colorectal tumor development and progression by inducing aerobic glycolysis and epithelial-mesenchymal transition.
Loss of ABHD5 promotes the aggressiveness of prostate cancer cells.
Lysophosphatidic acid acyltransferase ? (LPAAT?) promotes the tumor growth of human osteosarcoma.
Lysophosphatidic acid acyltransferase-beta (LPAAT-beta) is highly expressed in advanced ovarian cancer and is associated with aggressive histology and poor survival.
Lysophosphatidic acid acyltransferase-beta is a prognostic marker and therapeutic target in gynecologic malignancies.
Lysophosphatidic acid acyltransferase-beta: a novel target for induction of tumour cell apoptosis.
Macrophage ABHD5 suppresses NF-?B-dependent matrix metalloproteinase expression and cancer metastasis.
Oncogenic role of ABHD5 in endometrial cancer.
The structure and functions of human lysophosphatidic acid acyltransferases.
[Relationship between Lysophosphatide Acid Acyltransferase beta and Tumor - Review.]
Non-alcoholic Fatty Liver Disease
A novel mutation of ABHD5 gene in a Chanarin Dorfman patient with unusual dermatological findings.
Inherited non-alcoholic fatty liver disease and dyslipidemia due to monoallelic ABHD5 mutations.
Two cases of non-alcoholic fatty liver disease caused by biallelic ABHD5 mutations.
Obesity
Adipose-selective overexpression of ABHD5/CGI-58 does not increase lipolysis or protect against diet-induced obesity.
Congenital generalized lipodystrophy: significance of triglyceride biosynthetic pathways.
Transcriptomic and epigenetic changes in early liver steatosis associated to obesity: Effect of dietary methyl donor supplementation.
[Neutral lipid storage diseases and ATGL (adipose triglyceride lipase) and CGI-58/ABHD5 (alpha-beta hydrolase domain-containing 5) deficiency: myopathy, ichthyosis, but no obesity]
Osteosarcoma
Lysophosphatidic acid acyltransferase ? (LPAAT?) promotes the tumor growth of human osteosarcoma.
MicroRNA-24 inhibits osteosarcoma cell proliferation both in vitro and in vivo by targeting LPAAT?.
Silencing LPAAT? inhibits tumor growth of cisplatin-resistant human osteosarcoma in vivo and in vitro.
Ovarian Neoplasms
Clinical significance of combining salivary mRNAs and carcinoembryonic antigen for ovarian cancer detection.
Expression of lysophosphatidic acid acyltransferase beta (LPAAT-beta) in ovarian carcinoma: correlation with tumour grading and prognosis.
LPAAT-beta identifies aggressive ovarian cancer.
Lysophosphatidic acid acyltransferase-beta is a prognostic marker and therapeutic target in gynecologic malignancies.
Pancreatic Neoplasms
Identification of prognostic lipid droplet-associated genes in pancreatic cancer patients via bioinformatics analysis.
Polyneuropathies
Berardinelli-Seip syndrome patient with novel AGPAT2 splicesite mutation and concomitant development of non-diabetic polyneuropathy
Precursor Cell Lymphoblastic Leukemia-Lymphoma
[Lysophosphatidic acid acyltransferase ? gene expression in newly diagnosed leukemia patients].
Prostatic Neoplasms
ABHD5 suppresses cancer cell anabolism through lipolysis-dependent activation of the AMPK/mTORC1 pathway.
Loss of ABHD5 promotes the aggressiveness of prostate cancer cells.
Positive regulation of prostate cancer cell growth by lipid droplet forming and processing enzymes DGAT1 and ABHD5.
Protein Deficiency
Truncation of CGI-58 protein causes malformation of lamellar granules resulting in ichthyosis in Dorfman-Chanarin syndrome.
Pulmonary Disease, Chronic Obstructive
Gene and metabolite time-course response to cigarette smoking in mouse lung and plasma.
Sepsis
Interaction of lipopolysaccharide with a mammalian lyso-phosphatidate acyltransferase (LPAAT) transfected into E. coli, and effect of lisofylline on LPAAT transfected into mammalian cells.
Thymoma
Inherited lipodystrophies and hypertriglyceridemia.
Lipodystrophies: Disorders of adipose tissue biology.