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PEA15 encodes a death effector domain-containing protein, which is a major phosphoprotein in astrocytes, and an endogenous substrate for protein kinase C. Additionally we are shipping PEA15 Proteins (12) and PEA15 Kits (8) and many more products for this protein.
Showing 10 out of 105 products:
Human Polyclonal PEA15 Primary Antibody for FACS, IHC (p) - ABIN652463
Trencia, Perfetti, Cassese, Vigliotta, Miele, Oriente, Santopietro, Giacco, Condorelli, Formisano, Beguinot: Protein kinase B/Akt binds and phosphorylates PED/PEA-15, stabilizing its antiapoptotic action. in Molecular and cellular biology 2003
Show all 3 references for ABIN652463
Human Polyclonal PEA15 Primary Antibody for EIA, WB - ABIN453779
Sugiyama, Masuda, Shinoda, Nakamura, Tomita, Ishihama: Phosphopeptide enrichment by aliphatic hydroxy acid-modified metal oxide chromatography for nano-LC-MS/MS in proteomics applications. in Molecular & cellular proteomics : MCP 2007
Show all 2 references for ABIN453779
Cow (Bovine) Polyclonal PEA15 Primary Antibody for WB - ABIN2783293
Eckert, Böck, Tagscherer, Haas, Grund, Sykora, Herold-Mende, Ehemann, Hollstein, Chneiweiss, Wiestler, Walczak, Roth: The PEA-15/PED protein protects glioblastoma cells from glucose deprivation-induced apoptosis via the ERK/MAP kinase pathway. in Oncogene 2008
Human Polyclonal PEA15 Primary Antibody for IHC, ELISA - ABIN1531459
Wolford, Bogardus, Ossowski, Prochazka: Molecular characterization of the human PEA15 gene on 1q21-q22 and association with type 2 diabetes mellitus in Pima Indians. in Gene 2000
High PED expression is associated with esophageal carcinoma.
The nuclear translocation of SApErk1/ 2 apart from PEA-15 as an important mechanism to reverse senescence phenotype.
Latent HCMV infection of CD34 (show CD34 Antibodies) + cells protects cells from FAS (show FAS Antibodies)-mediated apoptosis through the cellular IL-10 (show IL10 Antibodies)/PEA-15 pathway.
New therapeutic targets based around PEA-15 and its associated interactions are now being uncovered and could provide novel avenues for treatment strategies in multiple diseases.
PED/PEA-15 overexpression is sufficient to block hydrogen peroxide-induced apoptosis in Ins-1E cells through a PLD-1 mediated mechanism
Omi/HtrA2 (show HTRA2 Antibodies) overexpression promotes hepatocellular carcinoma cell apoptosis and the ped/pea-15 expression level causes this difference of the Omi/HtrA2 (show HTRA2 Antibodies) pro-apoptotic marker in the various hepatocellular carcinoma cell lines
Results suggest that neurochemical adaptations of brain FADD (show FADD Antibodies), as well as its interaction with PEA-15, could play a major role to counteract the known activation of the mitochondrial apoptotic pathway in major depression
Data show that phosphoprotein enriched in astrocytes of 15 kDa (PEA-15) influences dephosphorylation of epidermal growth factor receptor (EGFR (show EGFR Antibodies)) via extracellular signal-regulated kinases ERK1/2 (show MAPK1/3 Antibodies) sequestration in the cytoplasm.
Tumor suppressor PEA15 is a regulator of genome integrity and is an integral component of the DNA damage response pathway.
Up-regulated chaperone-mediated autophagy activity characteristic of most types of cancer cell enhances oncogenesis by shifting the balance of PED function toward tumor promotion.
Data suggest that PEA-15 contributes to the specification of the cytokine pattern of activated Th cells, thus highlighting a potential new target to interfere with T cell functional polarization and subsequent immune response.
Activated astrocytes are known to clear the Abeta (show APP Antibodies) deposited in the extracellular milieu, which is why they play a key role in regulating the progression of Alzheimer's disease (AD).
Activation of peroxisome proliferator-activated receptor-gamma (PPARgamma (show PPARG Antibodies)) represses transcription of the ped/pea-15 gene.
The findings revealed a novel mechanism by which PEA-15 positively regulates Ras/ERK signaling and increases the proliferation of H-Ras-transformed epithelial cells through enhanced phospholipase D1 expression and activation.
PEA-15 did not differentiate and showed markedly enhanced autophagy. In these same cells, the autophagy inhibitor 3 (show PPP1R11 Antibodies)-methyladenine rescued TGF-beta1 (show TGFB1 Antibodies) effect on both autophagy and myogenesis, indicating that PEA-15 mediates TGF-beta1 (show TGFB1 Antibodies) effects in muscle.
Data suggest that PED/PEA-15 may affect fibroblast motility by a mechanism, at least in part, mediated by ERK1/2 (show MAPK1/3 Antibodies).
we propose that PEA-15 represents a novel point of convergence of the protein kinas C and MAPK/ERK (show MAPK1 Antibodies) pathways under gonadotropin releasing hormone stimulation
PEA-15 regulates T-cell proliferation
PEA-15 inhibits tumorigenesis in an MDA-MB-468 triple-negative breast cancer xenograft model through increased cytoplasmic localization of activated extracellular signal-regulated kinase.
This gene encodes a death effector domain-containing protein, which is a major phosphoprotein in astrocytes, and an endogenous substrate for protein kinase C. Studies using knockout mice suggest that this protein may protect astrocytes from TNF-induced apoptosis. This protein is also overexpressed in type 2 diabetes mellitus, where it may contribute to insulin resistance in glucose uptake.
phosphoprotein enriched in astrocytes 15
, Astrocytic phosphoprotein PEA-15
, 15 kDa phosphoprotein enriched in astrocytes
, Phosphoprotein enriched in astrocytes, 15kD
, astrocytic phosphoprotein PEA-15
, homolog of mouse MAT-1 oncogene
, phosphoprotein enriched in diabetes
, phosphoprotein enriched in astrocytes 15A
, mammary transforming gene 1