Browse our anti-ABHD5 (ABHD5) Antibodies

Human Abhydrolase Domain Containing 5 (ABHD5) interaction partners

1. ABHD5 is a potential therapeutic target against metastatic castration-resistant prostate cancer.

2. The results here report on three patients with mutations in the ichthyosis-related gene, ABHD5 involved in lipid metabolism, presenting with erythrokeratoderma.

3. Study report that although ABHD5 plays a tumor suppressor role in colorectal cancer (CRC) development and progression, it unexpectedly blunts the sensitivity of CRC cells to fluorouracil via promoting RNASET2-mediated autophagic uracil yield.

4. ABHD5 mutation is associated with Chanarin Dorfman Syndrome.

5. Study results suggest that ABHD5 functions to retain triglyceride, the substrate of PNPLA1, in the endoplasmic reticulum, the site of acylceramide production, and to present TG to PNPLA1. These findings reveal the molecular mechanism by which ABHD5 mutations cause ichthyosis symptoms in Chanarin-Dorfman syndrome.

6. novel homozygote deletion in exon 4 of ABHD5 causing Chanarin-Dorfman syndrome (CDS), a rare autosomal recessive metabolic disorder.

7. our findings indicate that inhibition of both DGAT1 and ABHD5 using siRNA leads to reduction in prostate cancer cell growth.

8. Prebinding CGI-58 with PI(3)P or PI(5)P did not alter its coactivation of ATGL in vitro. In summary, purified recombinant CGI-58 that is functional as an ATGL coactivator lacks LPAAT activity.

9. It is clear that CGI-58 can regulate TAG hydrolysis by activating the major TAG hydrolase adipose triglyceride lipase (ATGL), yet CGI-58 can also regulate lipid metabolism via mechanisms that do not involve ATGL.

10. ABHD5 possesses a PNPLA2-independent function in regulating autophagy and tumorigenesis.

11. These results indicate that HCV taps into the lipid droplet triglyceride reservoir usurping ABHD5 lipase cofactor function

12. Case Report: novel ABHD5 mutation, c.838C > T (p.Arg280*), in trans with p.Arg234* in a Chinese patient with very mild Dorfman-Chanarin syndrome.

13. Authors show that rat ATGL, coactivated by rat CGI-58, efficiently hydrolyzes triglycerides and retinyl ester.

14. novel ABHD5 truncating variant in a twenty nine month old female child, who presented with icthyosiform erythroderma.

15. simultaneous tryptophan alanine permutations in both arms abolish localization and activity of CGI-58 as opposed to tryptophan substitutions that occur in only one arm.

16. this study presents clinical and molecular data of four affected relatives with Chanarin-Dorfman syndrome homozygous for a N209X mutation in ABHD5, and provides a short review by comparing patients with N209X homozygous mutations to patients with other ABHD5 mutations.

17. PLIN5 was significantly colocated with ATGL, mitochondria and CGI-58, indicating a close association between the key lipolytic effectors in resting skeletal muscle.

18. -mediated phosphorylation of CGI-58 is required for dispersion of CGI-58 from perilipin 1A-coated lipid droplets

19. Abhd5 expression falls substantially and correlates negatively with malignant features in human colorectal cancer.

20. Findings indicate a molecular mechanisms by which lysophosphatidic acid acyltransferase CGI-58 regulates lipid homeostasis.

Mouse (Murine) Abhydrolase Domain Containing 5 (ABHD5) interaction partners

1. suppresses spermidine synthase-dependent spermidine production in tumour-associated macrophages and potentiates the growth of colorectal cancer

2. Mice lacking brown adipose tissue CGI-58 gene, a lipolytic activator essential for the stimulated lipid droplet lipolysis, have normal thermogenic capacity and are not cold sensitive.

3. Prebinding CGI-58 with PI(3)P or PI(5)P did not alter its coactivation of ATGL in vitro. In summary, purified recombinant CGI-58 that is functional as an ATGL coactivator lacks LPAAT activity.

4. CGI-58 regulates hepatic neutral lipid storage and inflammation in the genetic absence of ATGL.

5. ABHD5 possesses a PNPLA2-independent function in regulating autophagy and tumorigenesis.

6. omega-O-AcylCer and CLE formation critically depend on CGI-58 expression in differentiated keratinocytes.

7. These results demonstrate that macrophage CGI-58 enhances PPAR-gamma signaling and thus suppresses inflammatory responsiveness and mitochondrial dysfunction in macrophages.

8. Here, we identify synthetic ligands that release ABHD5 from PLIN1 or PLIN5 without PKA activation and rapidly activate adipocyte and muscle lipolysis.

9. we identify adipocyte-type fatty acid-binding protein (A-Fabp) and other members of the fatty acid-binding protein (Fabp) family as interaction partners of Cgi-58.

10. Data (including data from studies in atherosclerotic knockout mice) suggest CGI58-deficient macrophages store-up triglyceride-rich droplets and have reduced phagocytic capacity, comparable to Atgl- (adipose triglyceride lipase-)deficient macrophages.

11. -mediated phosphorylation of CGI-58 is required for dispersion of CGI-58 from perilipin 1A-coated lipid droplets

12. Muscle CGI-58 deficiency causes cardiac dysfunction and fat deposition in oxidative muscles but induces a series of favorable metabolic changes in mice fed a high-fat diet.

13. intestinal CGI-58 is required for efficient postprandial lipoprotein-TG secretion and for maintaining hepatic and plasma lipid homeostasis.

14. CGI-58 transgenic/ApoE-/- mice exhibited an anti-atherosclerosis phenotype compared with wild type (WT) controls (CGI-58 WT/ApoE-/-), illustrated by less plaque area in aortic roots.

15. The anti-lipolytic activity of the HCV core protein alters ATGL binding to CGI-58 and enhances the association of both proteins with lipid droplets.

16. These data thus identified a vicious cycle (IL-1beta-SOCS3-FOXO1-IL-1beta) that amplifies IL-1beta secretion and is initiated by CGI-58 deficiency-induced activation of the NLRP3 inflammasome in macrophages.

17. Perilipins 2 and 3 lack a carboxy-terminal domain present in perilipin 1 involved in sequestering ABHD5 and suppressing basal lipolysis.

18. The CGI-58 deficiency in the liver directly causes not only hepatic steatosis but also steatohepatitis and fibrosis.

19. These results suggest that reduced ATGL and CGI-58 expression and increased TG synthesis may exacerbate myocardial steatosis and oxidative stress, thereby promoting cardiac apoptosis in diabetic mice.

20. functional muscle lipolysis depends on both CGI-58 and ATGL

Pig (Porcine) Abhydrolase Domain Containing 5 (ABHD5) interaction partners

1. These findings suggest that CGI-58 may be a new target for enhancing the quality of pork products as well as offering the potential of CGI-58 for human obesity treatment.