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PDCD5 encodes a protein that is upregulated during apoptosis where it translocates rapidly from the cytoplasm to the nucleus. Additionally we are shipping PDCD5 Antibodies (78) and PDCD5 Kits (6) and many more products for this protein.
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DKK-1 (show DKK1 Proteins) and PDCD5 can be independent predictors of overall survival in patients suffering from chondrosarcoma.
Data show that lower serum levels of programmed cell death protein 5 (PDCD5) protein were identified in the gastric cancer patients that with CD133(+) fraction more than 1.6 %.
Endogenous PDCD5 overexpression accelerated multiple myeloma cell apoptosis under dexamethasone treatment.
Studies indicate that programmed cell death 5 (PDCD5) interacts with the tumor protein p53 (p53 (show TP53 Proteins)) pathway to promote cell apoptosis.
This review describes what is known about PDCD5 and its cellular functions. [review]
The results suggest a role of PDCD5 in the regulation of p53 (show TP53 Proteins) function but unrelated to cell cycle arrest or apoptosis, at least in the cell types investigated.
PDCD5 selectively mediates HDAC3 (show HDAC3 Proteins) dissociation from p53 (show TP53 Proteins), which induces HDAC3 (show HDAC3 Proteins) cleavage and ubiquitin-dependent proteasomal degradation. This is a a mechanism for p53 (show TP53 Proteins) activation via PDCD5-dependent HDAC3 (show HDAC3 Proteins) decay under genotoxic stress conditions.
PDCD5 expression is negatively correlated with disease progression and stage in ovarian cancer.
These findings uncovered an apoptotic signaling cascade linking YAF2 (show YAF2 Proteins), PDCD5, and TP53 (show TP53 Proteins) during genotoxic stress responses.
Transgenic mice with systemic overexpression of human PDCD5 were protected from cardiac remodeling.
These data demonstrate an association between level of PDCD5 and asthma severity and indicate that PDCD5 may play a role in allergic asthma.
PDCD5 gene knockout mice presented obvious improved brain blood flow, improved neurological behavior and decreased cerebral infarction compared with wild type mice. mice lacking PDCD5 had no changes in the expression of VHL (show VHL Proteins) and have slighter increases in the expression of HIF-1alpha (show HIF1A Proteins) and BNIP3 (show BNIP3 Proteins), suggesting that PDCD5 may regulate apoptosis and autophagy through VHL (show VHL Proteins)-HIF-1alpha (show HIF1A Proteins)-BNIP3 (show BNIP3 Proteins) pathway.
It is implied that overexpression of PDCD5 causes the increase in caspase-3 (show CASP3 Proteins) activity and the subsequent increase of apoptosis in cochlear hair cells and SGNs, and thereby plays a role in the pathogenesis of presbycusis.
PDCD5 activity in T cells suppresses autoimmunity by modulating regulatory T-cells.
The expression levels of PDCD5 and caspase 3 (show CASP3 Proteins) in the cochlea of C57 mice increase with age.
Suppresses the pathogenicity of transplanted mouse erythroleukemia (MEL (show RAB8A Proteins)) cells in mice.
This gene encodes a protein that is upregulated during apoptosis where it translocates rapidly from the cytoplasm to the nucleus. The encoded protein may be an important regulator of K(lysine) acetyltransferase 5 (a protein involved in transcription, DNA damage response and cell cycle control) by inhibiting its proteasome-dependent degradation. Pseudogenes have been identified on chromosomes 5 and 12
programmed cell death protein 5
, programmed cell death 5
, hypothetical protein
, TF-1 cell apoptosis-related protein 19
, TF1 cell apoptosis-related gene 19
, TFAR19 novel apoptosis-related
, TF-1 cell apoptosis related gene-19 protein