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Chicken Monoclonal PTGES3 Primary Antibody for FACS, ICC - ABIN152733
Casanelles, Gozzelino, Marqués-Fernández, Iglesias-Guimarais, Garcia-Belinchón, Sánchez-Osuna, Solé, Moubarak, Comella, Yuste: NF-κB activation fails to protect cells to TNFα-induced apoptosis in the absence of Bcl-xL, but not Mcl-1, Bcl-2 or Bcl-w. in Biochimica et biophysica acta 2013
Show all 4 Pubmed References
The Hsp90 (show HSP90 Antibodies) independence of the interaction between p23 and p53 (show TP53 Antibodies) DNA-binding domain, together with the competition of p23 versus DNA for p53 (show TP53 Antibodies), raises the intriguing possibility that p23, like other small charged proteins, may affect p53 (show TP53 Antibodies) in hitherto unknown ways.
dysregulation of GR, MR, FKBP5 (show FKBP5 Antibodies), and PTGES3 in autistic spectrum disorder (ASD (show ARSD Antibodies)) and suggest a possible role of inflammation in altered GR function in ASD (show ARSD Antibodies).
increased p23 expression may allow cells to acquire a more aggressive phenotype, contributing to disease progression
Even if p23 predominantly binds the Hsp90 (show HSP90 Antibodies) dimer, p23 is also able to interact with Hsp90 (show HSP90 Antibodies) oligomers, shifting the Hsp90 (show HSP90 Antibodies) dimer-oligomers equilibrium toward dimer.
FKBP4 (show FKBP4 Antibodies), p23, and Aha1 (show AHSA1 Antibodies) cooperatively regulate the progression of hAgo2 (show EIF2C2 Antibodies) through the chaperone cycle.
p23 recruits PHD2 (show EGLN1 Antibodies) to the HSP90 (show HSP90 Antibodies) machinery to facilitate HIF-1alpha (show HIF1A Antibodies) hydroxylation
The effects of p23 on androgen receptor (AR (show AR Antibodies)) activity are at least partly HSP90 (show HSP90 Antibodies) independent, a mutant form of p23, unable to bind HSP90 (show HSP90 Antibodies), increases AR activity.
p23 co-chaperone protects the aryl hydrocarbon receptor (show AHR Antibodies) from degradation
As an anti-apoptotic factor, p23 is able to be a potential target for anti-leukemic therapy.
Patients with severe Alzheimer disease displayed a consistent reduction in brain p23 levels. Cleavage product p19 was not seen in AD brain samples.
Skin differentiation is impaired, and both apoptosis and cell proliferation are augmented in the absence of p23 (show CDK5R1 Antibodies); the consequences are a severe thinning of the stratum corneum and reduced numbers of hair follicles. Since the phenotype of p23 (show CDK5R1 Antibodies)-null embryos is strikingly similar to that of embryos lacking the glucocorticoid receptor (show NR3C1 Antibodies), a paradigmatic Hsp90 (show HSP90 Antibodies)-p23 (show CDK5R1 Antibodies) client protein, we investigated glucocorticoid signaling.
Results identified two proteins P23 (show CDK5R1 Antibodies) and HCLS1 (show HCLS1 Antibodies), which were not known as RNA-binding proteins, exhibiting RNA-binding activity.
we report the generation of transgenic mouse lines that overexpress wild-type p23 (show CDK5R1 Antibodies) or uncleavable p23 (show CDK5R1 Antibodies)
Data support a model in which p23 and GCN5 regulate diverse multistep pathways by controlling the longevity of protein-DNA complexes.
p23 (show CDK5R1 Antibodies) co-chaperone protects the aryl hydrocarbon receptor (show AHR Antibodies) from degradation
Cleavage product p19 was not seen in brain samples from a mouse model of Alzheimer disease, but p23 and p19 were seen in hypoxic cultured cells experienceing endoplasmic reticulum stress.
In cytosol only one protein called p23 (show CDK5R1 Antibodies) hsp90 (show HSP90 Antibodies) binds to Bax (show BAX Antibodies) but the binding protein does not affect the subcellular localization and pro-apoptotic activity of Bax (show BAX Antibodies).
The p23 cochaperone of Hsp90, which plays a major role in glucocorticoid receptor folding and function, associates with influenza virus polymerase.
Overexpression of p23 (show CDK5R1 Antibodies) contributes to the development of hydronephrosis through the upregulation of the aryl hydrocarbon receptor (show AHR Antibodies) pathway in vivo.
prostaglandin E synthase (show PTGES Antibodies) (cPGES/p23) acts as a regulatory factor for expression of a PGE2-inactivating enzyme, 15-PGDH (show HPGD Antibodies)
Zebrafish cytosolic (c) PGES (show PTGES Antibodies)-1 and COX-1 (show PTGS1 Antibodies) were coordinately expressed in the inner ear, the pronephros, and intestine.
Molecular chaperone that localizes to genomic response elements in a hormone-dependent manner and disrupts receptor- mediated transcriptional activation, by promoting disassembly of transcriptional regulatory complexes (By similarity).
, cytosolic prostaglandin E synthase
, cytosolic prostaglandin E2 synthase
, progesterone receptor complex p23
, prostaglandin E synthase 3
, telomerase-binding protein p23
, unactive progesterone receptor, 23 kD
, prostaglandin E synthase 3 (cytosolic)
, hsp90 co-chaperone
, p23 cochaperone
, sid 3177
, telomerase binding protein, p23
, prostaglandin-E synthase 3