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PHLDA1 encodes an evolutionarily conserved proline-histidine rich nuclear protein. Zusätzlich bieten wir Ihnen PHLDA1 Antikörper (48) und und viele weitere Produktgruppen zu diesem Protein an.
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Our study negatively correlates expression of PHLDA1 and Aurora A (zeige AURKA Proteine) in IMR-32 cells and sheds new light on functions of PHLDA1 in the neuroblastoma (zeige ARHGEF16 Proteine) 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 (zeige NFKB1 Proteine)-miR (zeige MLXIP Proteine)-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 (zeige AURKA Proteine) by the therapeutic antibody is associated with decreased levels of MYCN (zeige MYCN Proteine) protein in cytoplasm, and induced expression of PHLDA1 and P53 (zeige TP53 Proteine) 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 (zeige CA2 Proteine)+) 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 (zeige AURKA Proteine) 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 (zeige TLR4 Proteine)-mediated proliferation and cell cycle progression, and which increase our understanding of the interaction mechanism between LPS (zeige TLR4 Proteine) and macrophages.
The JAK2 (zeige JAK2 Proteine)-ERK1/2-STAT3 (zeige STAT3 Proteine) pathway is an important signaling pathway for regulation of PHLDA1 expression.
TDAG51 has a protective role in oxidative stress-induced (zeige SQSTM1 Proteine) cell death in mouse embryonic fibroblasts.
Our results suggest that the balance between the cell survival and death signals mediated by HSP70 (zeige HSP70 Proteine) and TDAG51, respectively, may be disturbed by the altered expression of HSF1 (zeige HSF1 Proteine) 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 (zeige ITGA2 Proteine) and ITGA6 (zeige ITGA6 Proteine), 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