Aperçu des produits pour anti-PLA2G16 (PLA2G16) Anticorps

Human HRAS-Like Suppressor 3 (PLA2G16) interaction partners

1. study uncovers two competing processes triggered by Picornaviridae virus entry: activation of a pore-activated clearance pathway and recruitment of a PLA2G16 phospholipase to enable genome release

2. Demonstrate increased PLA2G16 expression activates the MAPK pathway to enhance osteosarcoma metastasis.

3. our results revealed that H-rev107 is also involved in lipid accumulation in liver cells through the POR pathway via its PLA2 activity.

4. Results show that osteosarcoma patients with metastasis showed higher expression of PLA2G16 at both the mRNA and protein levels and shorter overall survival suggesting it as significant prognostic factor for poor outcome.

5. suggest a novel regulatory mechanism for peroxisome biogenesis through the interaction between Pex19p and PLA/AT-3

6. the flexible main loop of H-REV107, but not that of TIG3, is critical for its NTD to modulate its CTD in inducing cell death.

7. crystal structure of the HRASLS3-LRAT chimeric enzyme in a thioester catalytic intermediate state revealed a major structural rearrangement accompanied by three-dimensional domain swapping dimerization not observed in native HRASLS

8. several mutant p53 proteins bind the Pla2g16 promoter at E26 transformation-specific (ETS) binding motifs and knockdown of ETS2 suppressed mutant p53 induction of Pla2g16.

9. Our study further suggests that the PLA/AT activity of H-rev107 may play an important role in H-rev107-mediated RAS suppression.

10. an alternate mechanism for AdPLA in promoting adipose tissue lipolysis that is not contingent on the release of arachidonic acid and that is compatible with its combined PLA(1)/A(2) activity

11. Data show that acyl-modified forms of HRAS-like tumor suppressors HRASLS2 and HRASLS3 mimicking lipolytic activity of lecithin retinol acyltransferase LRAT.

12. role of PKC isoenzymes in PP2A and HRSL3(H-REV107-1) tumor suppressor-dependent cell death induction in ovarian carcinoma cell line; verified contribution to PP2A- and HRLS3-dependent apoptosis for PKCzeta suggesting a proapoptotic function of this kinase

13. AdPLA ablation increases lipolysis and prevents obesity induced by high-fat feeding or leptin deficiency.

14. Identification and functional characterization of adipose-specific phospholipase A2 (AdPLA)

15. Contact inhibition of growth and growth arrest caused by histone deacetylase inhibitors probably use the same mechanism to stimulate H-rev107 expression via histone acetylation in NIH3T3 cells

16. H-REV107-1 is deficient in its function as a tumor suppressor in non-small cell lung carcinomas.

Mouse (Murine) HRAS-Like Suppressor 3 (PLA2G16) interaction partners

1. several mutant p53 proteins bind the Pla2g16 promoter at E26 transformation-specific (ETS) binding motifs and knockdown of ETS2 suppressed mutant p53 induction of Pla2g16.

2. H-rev107, through PTGDS, suppressed cell migration and invasion. Data suggest that the PGD2-cAMP-SOX9 signal pathway might play an important role in H-rev107-mediated cancer cell invasion in testes.

3. H-rev107 interferes with the biosynthesis of ether-type lipids and is responsible for the dysfunction of peroxisomes in H-rev107-expressing cells.

4. identification of an Sp1/Sp3-binding GC-box required for the transcription of H-rev107 (H-rev107)

5. study found that AdPLA that was previously known as H-Rev-107/HRASLS3 is an adipose-specific, calcium-dependent histidine PLA2

6. HRASLS3 as one of the downstream effectors of PPARgamma action in adipogenesis.

Cow (Bovine) HRAS-Like Suppressor 3 (PLA2G16) interaction partners

1. Single nucleotide polymorphisms in the adipose specific phospholipase A2 are associated with growth traits in cattle.