To Browse through specific   lists, the search terms can   be prefixed with following   letters:
   d:  for diseases
   m: for molecules
   p:  for pathways
    c:  for cell lines
   v:  for interaction terms

*Search for genes, compounds, disease, cell/cell lines, organ, disease, pathway, process. (E.g Breast Neoplasms AND EGFR)

Modules
Statistics Flexibility to integrate Publication and
Posters Case Study Collaboration Testimonials Press Release
Interaction IDMol ATypeSpeciesVerbNatureMol BTypeSpecies
34098TNFProteinHomo sapiens-eIncreases expressionindirectPLA2G4ARNAHomo sapiens
Phospholipase A(2) (PLA(2)) is a growing family of enzymes that may play a major role in inflammation / The cells were stimulated with TNF-alpha or IFN-gamma for different lengths of time (1, 4, 18, and 48 h), and the mRNA levels of the different PLA(2) types were determined by reverse transcriptase-PCR (RT-PCR) and normalized to those of the housekeeping gene, GAPDH. In both cell lines, TNF-alpha increased the expression of PLA(2) IVA and IVC, and IFN-gamma increased the expression of PLA(2) IIA and IID.
Disease
85680CHRM2ProteinHomo sapiens-eIncreases activityindirectPLA2G4AProteinHomo sapiens-e
The pathway initiated by m2 receptors involved sequential activation of Gbetagamma(i3), phosphatidylinositol (PI)3-kinase, Cdc42, and Rac1, p21-activated kinase (PAK1), p38 mitogen-activated protein (MAP) kinase, and cPLA(2), and phosphorylation of cPLA(2) at Ser(505).
Regulator
85681CHRM2ProteinHomo sapiens-eIncreases phosphorylationindirectPLA2G4AProteinHomo sapiens-e
The pathway initiated by m2 receptors involved sequential activation of Gbetagamma(i3), phosphatidylinositol (PI)3-kinase, Cdc42, and Rac1, p21-activated kinase (PAK1), p38 mitogen-activated protein (MAP) kinase, and cPLA(2), and phosphorylation of cPLA(2) at Ser(505).
Structure
Regulator
127252CalciumSmall moleculeSmall moleculeIncreases expressionindirectPLA2G4AProteinHomo sapiens
This implies that intracellular Ca(2+) level is the key factor for induction of cPLA(2) activity and thapsigargin-elicited ERK activation itself is substantially sufficient for cPLA(2) activation upon intracellular Ca(2+) increase.
138183PLA2G4AProteinHomo sapiensIncreases activityindirectPPARGProteinHomo sapiens
Overexpression of cPLA(2), but not group IIA sPLA(2) in the HepG2 cells, caused a significantly increased PPAR-alpha/gamma-mediated reporter activity. / Antisense inhibition of cPLA(2) resulted in a significantly decreased PPAR-alpha/gamma activity. The PPAR-alpha/gamma-induced gene transcription in the HepG2 cells was inhibited by the cPLA(2) inhibitors methyl arachidonyl fluorophosphonate and arachidonyltrifluoromethyl ketone, but not by the sPLA(2) inhibitor LY311727. / The cPLA(2)-mediated PPAR activation was likely mediated by arachidonic acid and prostaglandin E(2). / The cPLA(2) thus may represent a potential therapeutic target for the control of PPAR-related liver and metabolic disorders such as obesity, lipid metabolic disorders, diabetes mellitus, and atherosclerosis.
Disease
Regulator
220370NF-kappa-BMulti subunitHomo sapiensIncreases activitydirectPLA2G4ADNAHomo sapiens-e
Activation of cPLA2 is required for leukotriene D4-induced proliferation in colon cancer cells. / Here we demonstrate, for the first time that in both Int 407 (a non-transformed human intestinal epithelial cell line) and Caco-2 cells (a human colorectal carcinoma cell line), cytosolic phospholipase A(2)alpha (cPLA(2)alpha) is activated and translocates to the nucleus upon LTD(4) stimulation via a calcium-dependent mechanism that involves activation of protein kinase C (PKC), and the mitogen-activated protein kinases ERK1/2 and p38. We also show with a cPLA(2)alpha promoter luciferase assay, that LTD(4) induces an increase in the transcriptional activity of cPLA(2)alpha via activation of cPLA(2)alpha and the transcription factor NFkappaB. / The present data reveal that cPLA(2)alpha, an important intracellular signal activated by inflammatory mediators, is an important regulator of colon tumor growth.
Disease

Home · About Us · FAQ · Statistics · Contact Us · Register Now
© Copyright 2009 Molecular Connections Pvt. Ltd. All rights reserve. www.molecularconnections.com