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PHLDA1 encodes an evolutionarily conserved proline-histidine rich nuclear protein. Additionally we are shipping PHLDA1 Antibodies (48) and and many more products for this protein.
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Our study negatively correlates expression of PHLDA1 and Aurora A (show AURKA Proteins) in IMR-32 cells and sheds new light on functions of PHLDA1 in the neuroblastoma (show ARHGEF16 Proteins) 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 (show NFKB1 Proteins)-miR (show MLXIP Proteins)-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 (show AURKA Proteins) by the therapeutic antibody is associated with decreased levels of MYCN (show MYCN Proteins) protein in cytoplasm, and induced expression of PHLDA1 and P53 (show TP53 Proteins) 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 (show CA2 Proteins)+) 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 (show AURKA Proteins) in breast cancer
The data presented herein demonstrate TDAG51 expression to be upregulated in damaged skeletal muscle and its absence attenuates the early phases of muscle regeneration.
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 (show TLR4 Proteins)-mediated proliferation and cell cycle progression, and which increase our understanding of the interaction mechanism between LPS (show TLR4 Proteins) and macrophages.
The JAK2 (show JAK2 Proteins)-ERK1/2-STAT3 (show STAT3 Proteins) pathway is an important signaling pathway for regulation of PHLDA1 expression.
TDAG51 has a protective role in oxidative stress-induced (show SQSTM1 Proteins) cell death in mouse embryonic fibroblasts.
Our results suggest that the balance between the cell survival and death signals mediated by HSP70 (show HSP70 Proteins) and TDAG51, respectively, may be disturbed by the altered expression of HSF1 (show HSF1 Proteins) 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 (show ITGA2 Proteins) and ITGA6 (show ITGA6 Proteins), and contributes to intestinal tumorigenesis
TDAG51 is induced by homocysteine, promotes detachment-mediated PCD, 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