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PHLDA1 encodes an evolutionarily conserved proline-histidine rich nuclear protein. De plus, nous expédions PHLDA1 Anticorps (48) et PHLDA1 Protéines (5) et beaucoup plus de produits pour cette protéine.
Our study negatively correlates expression of PHLDA1 and Aurora A (Montrer AURKA Kits ELISA) in IMR-32 cells and sheds new light on functions of PHLDA1 in the neuroblastoma (Montrer ARHGEF16 Kits ELISA) tumor cells, suggesting its role as a pro-apoptotic protein
Suggest decreased expression of PHLDA1 may play an important role in tumor progression, and may become a new adjunct biomarker in the prognosis in gastric adenocarcinoma.
Data suggest that high PHLDA1 expression is controlled through an ER-NFkappaB (Montrer NFKB1 Kits ELISA)-miR (Montrer MLXIP Kits ELISA)-181 regulatory axis and may contribute to a poor clinical outcome in patients with ER+ breast tumors by enhancing stem-like properties in these tumors.
PHLDA1 expression is a useful addition in differentiating trichoblastoma and basal cell carcinoma.
A role for PHLDA1 as an apoptosis suppressor in oral cancer cells.
Data show that downregulation of aurora A kinase (Montrer AURKA Kits ELISA) by the therapeutic antibody is associated with decreased levels of MYCN (Montrer MYCN Kits ELISA) protein in cytoplasm, and induced expression of PHLDA1 and P53 (Montrer TP53 Kits ELISA) proteins.
The follicular stem cell marker PHLDA1 (TDAG51) indicates that most basaloid tumors in nevus sebaceus are basal cell carcinomas and not trichoblastomas.
PHLDA1 differentiates between desmoplastic trichoepithelioma and morpheaform basal cell carcinoma but shows variable staining in microcystic adnexal carcinoma.
the release of Ca(2 (Montrer CA2 Kits ELISA)+) from endoplasmic reticulum stores mediates epithelial-to-mesenchymal transition in human proximal tubular epithelium via the induction of TDAG51
crucial negative regulator and effector of Aurora A kinase (Montrer AURKA Kits ELISA) in breast cancer
PHLDA1 plays a critical role in the development of progressive lung contusion and subsequent inflammation.
These findings suggested that TDAG51 up-regulation is a dependent event during LPS (Montrer TLR4 Kits ELISA)-mediated proliferation and cell cycle progression, and which increase our understanding of the interaction mechanism between LPS (Montrer TLR4 Kits ELISA) and macrophages.
The JAK2 (Montrer JAK2 Kits ELISA)-ERK1/2 (Montrer MAPK1/3 Kits ELISA)-STAT3 (Montrer STAT3 Kits ELISA) pathway is an important signaling pathway for regulation of PHLDA1 expression.
TDAG51 has a protective role in oxidative stress-induced (Montrer SQSTM1 Kits ELISA) cell death in mouse embryonic fibroblasts.
Our results suggest that the balance between the cell survival and death signals mediated by HSP70 (Montrer HSP70 Kits ELISA) and TDAG51, respectively, may be disturbed by the altered expression of HSF1 (Montrer HSF1 Kits ELISA) during the progression of disease in this amyotropic lateral sclerosis model.
TDAG51 is involved in energy homeostasis at least in part by regulating lipogenesis in liver and white adipose tissue.
PHLDA1 expression marks the putative epithelial stem cells, downregulates ITGA2 (Montrer ITGA2 Kits ELISA) and ITGA6 (Montrer ITGA6 Kits ELISA), and contributes to intestinal tumorigenesis
TDAG51 is induced by homocysteine, promotes detachment-mediated PCD (Montrer PCBD1 Kits ELISA), and contributes to the development of atherosclerosis observed in hyperhomocysteinemia
This gene encodes an evolutionarily conserved proline-histidine rich nuclear protein. The encoded protein may play an important role in the anti-apoptotic effects of insulin-like growth factor-1.
, PQR protein
, T-cell death-associated gene 51 protein
, apoptosis-associated nuclear protein
, pleckstrin homology-like domain family A member 1
, proline- and glutamine-rich protein
, proline- and histidine-rich protein
, proline-histidine rich protein
, T-cell death associated