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displays increased expression in response to stress [RGD, Feb 2006].. Additionally we are shipping Tumor Protein P53 Inducible Nuclear Protein 1 Antibodies (100) and and many more products for this protein.
These data provide evidence that the TP53INP1 gene prevents metabolic syndrome, through a mechanism involving prevention of oxidative stress by mitochondrial homeostasis regulation.
Nanog enhances miR-17/92 cluster expression that in turn targets Trp53inp1, thus contributing to release neural stem cell self-renewal constraints.
TP53INP1 loss of expression contributes to pancreatic cancer formation in a conditional KrasG12D mouse model.
these data emphasize the role of TP53INP1 in protection against cell injury
Data show that induction of the stress-induced proteins (SIPs) SIP18 and SIP27, in human- and mouse-derived cell lines, is absent from cells with deleted, mutated or inactive p53 (show TP53 ELISA Kits), suggesting that regulation of SIP (show CACYBP ELISA Kits) gene expression is dependent on p53 (show TP53 ELISA Kits).
TP53INP1s are functionally associated with p73 (show ARHGAP24 ELISA Kits) to regulate cell cycle progression and apoptosis.
Tumor protein 53-induced nuclear protein 1 is a potential target for the prevention of colorectal cancer in patients with inflammatory bowel disease[Tumor protein 53-induced nuclear protein 1]
Low TP53INP1 expression is associated with Metastasis of Hepatocellular Carcinoma.
Negative TP53INP1 protein levels correlated with a poor outcome in pediatric ependymoma. Direct binding of miR (show MLXIP ELISA Kits)-124-3p to its target TP53INP1 is demonstrated.
Results showed that TP53INP1 and E-cadherin (show CDH1 ELISA Kits) mRNA and protein were significantly down-regulated in glioma tumors and positively correlated with higher grade and poor survival. Also, the study provides evidence that TP53INP1 3'-UTR (show UTS2R ELISA Kits) could inhibit the epithelial-mesenchymal transition, thus hindering the migration and invasion of glioma via acting as a competitive endogenous RNA for E-cadherin (show CDH1 ELISA Kits).
miR (show MLXIP ELISA Kits)-205/TP53INP1 mediated autophagy pathway might be an important molecular mechanism regulating radiosensitivity of prostate cancer cells
silencing of TP53inp1 leads radiation induced autophagy impairment and induces accumulation of damaged mitochondria in primary human fibroblasts.
MicroRNA205 promotes the tumorigenesis of nasopharyngeal carcinoma through targeting TP53INP1 protein.
FOXP1 (show FOXP1 ELISA Kits), TP53INP1, TNFAIP3 (show TNFAIP3 ELISA Kits), and TUSC2 (show TUSC2 ELISA Kits) were identified as miR (show MLXIP ELISA Kits)-19a targets.
GWAS identifies TP53INP1 as new susceptibility gene for Alzheimer's disease.
TP53INP1 SUMOylation is essential for the regulation of p53 (show TP53 ELISA Kits) activity induced by oxidative stress.
TGFB1 (show TGFB1 ELISA Kits) induced miR (show MLXIP ELISA Kits)-155 regulates TP53INP1 expression, epithelial-mesenchymal transition and acquisition of a stem cell phenotype.
displays increased expression in response to stress
tumor protein p53-inducible nuclear protein 1
, tumor protein p53 inducible nuclear protein 1
, p53-dependent damage-inducible nuclear protein 1
, stress induced protein
, stress-induced protein
, thymus expressed acidic protein
, thymus-expressed acidic protein
, p53-inducible p53DINP1
, transformation related protein 53 inducible nuclear protein 1