Disease relevance of TP53INP1

• CONCLUSION: TP53INP1-positive rate decreases with the progression of gastric cancer [1].
• TP53INP1 expression was significantly decreased (43.9%) in poorly differentiated adenocarcinoma compared with well or moderately differentiated adenocarcinoma (81.6%) [1].
• We report here that TP53INP1 expression is induced during experimental acute pancreatitis in p53-/- mice and in cisplatin-treated p53-/- mouse embryo fibroblasts (MEFs) [2].
• The TP53INP1 expression level was inversely linked to tumor size, positive lymph node metastasis, high histological grade and aberrant p53 expression [3].
• Stress-induced premature senescence in hTERT-expressing ataxia telangiectasia fibroblasts [4].

Psychiatry related information on TP53INP1

• Stress-induced enhancement of fear learning: an animal model of posttraumatic stress disorder [5].
• Stress-induced hallucinations [6].
• Stress-induced and sympathetically-mediated electrocardiographic and circulatory variations in the primary hyperkinetic heart syndrome [7].
• Stress-induced physiological reactivity has been shown to correlate with indexes of pain sensitivity, but it has not been demonstrated whether such reactivity can affect subsequent levels of pain threshold, tolerance and self-reported severity [8].
• Stress-induced blood pressure responses, together with measures of sympathetic nervous system activity (11%) and psychological factors (6%), were relatively weak predictors of subsequent pressure classification [9].

High impact information on TP53INP1

• Stress-induced immunological reactions to exercise have stimulated much research into stress immunology and neuroimmunology [10].
• Activation of Glucosidase via Stress-Induced Polymerization Rapidly Increases Active Pools of Abscisic Acid [11].
• Stress-induced immunomodulation: implications for infectious diseases [12]?
• Stress-induced cortical release may be preserved despite notable abnormalities in regulation of cortisol secretion by diurnal and feedback-mediated mechanisms [13].
• Stress-induced cortisol release in hypothalamic hypoadrenalism [13].

Chemical compound and disease context of TP53INP1

• Stress-induced myocardial ischemia, as assessed by thallium-201 scintigraphy, was decreased by 54% (p less than .05) despite higher myocardial oxygen consumption [14].
• Stress-induced gastroduodenal lesions and total parenteral nutrition in critically ill patients: frequency, complications, and the value of prophylactic treatment. A prospective, randomized study [15].
• Stress-induced increases in plasma E may result in prejunctional uptake of E in nerve terminals with release of E as a cotransmitter with NE--i.e., facilitation of NE release leading to postjunctional vasoconstriction and hypertension [16].
• Stress-induced left ventricular dysfunction in silent and symptomatic myocardial ischemia during dobutamine stress test [17].
• Stress-induced hemodynamic and hemostatic changes in patients with systemic hypertension: effect of verapamil [18].

Biological context of TP53INP1

• Although a TP53INP1s and HIPK2 additive effect was observed on apoptosis, G1 arrest was weaker when HIPK2 was transfected together with TP53INP1 [19].
• TP53INP1 protein negativity is significantly associated with aggressive pathological phenotypes of gastric cancer [1].
• AIM: Overexpression of tumor protein p53-induced nuclear protein 1 (TP53INP1) induces G1 cell cycle arrest and increases p53-mediated apoptosis [1].
• TP53INP1 was shown to mediate phosphorylation of p53 on serine 46 [20].
• Assignment of tumor protein p53 induced nuclear protein 1 (TP53INP1) gene to human chromosome band 8q22 by in situ hybridization [21].

Anatomical context of TP53INP1

• RESULTS: Diffuse and intense TP53INP1 expression was observed in the normal mammary gland [3].
• Using the differential display method combined with a cell line that carries a well-controlled expression system for wild-type p53, we isolated a p53-inducible gene, termed p53DINP1 (p53-dependent damage-inducible nuclear protein 1) [22].
• Stress-induced activation of the p53 tumor suppressor in leukemia cells and normal lymphocytes requires mitochondrial activity and reactive oxygen species [23].
• Stress-induced norepinephrine release in the hypothalamic paraventricular nucleus and pituitary-adrenocortical and sympathoadrenal activity: in vivo microdialysis studies [24].
• Stress-induced structural remodeling in the adult hippocampus, involving debranching and shortening of dendrites and suppression of neurogenesis, provides a cellular basis for understanding the impairment of neural plasticity in the human hippocampus in depressive illness [25].

Associations of TP53INP1 with chemical compounds

• The PAP mRNA expression was decreased after being treated with gemcitabine, whereas the TP53INP1 mRNA was increased by the gemcitabine treatment [26].
• Stress-induced premature senescence (SIPS) occurs after many different sublethal stresses including H(2)O(2), hyperoxia, or tert-butylhydroperoxide [27].
• Stress-induced release of tryptase and histamine, but not of prostaglandin D2 and water flux, was greater in food-allergic patients than in healthy volunteers [28].
• Stress-induced cocaine craving and hypothalamic-pituitary-adrenal responses are predictive of cocaine relapse outcomes [29].
• Stress-induced epinephrine release, measured in urine, was less in a group of 17 nonalcoholic adoptee probands, aged 18 to 36 years, with alcoholic biologic relatives than in 12 similar controls with no alcoholic relatives [30].

Enzymatic interactions of TP53INP1

• Furthermore, the protein complex interacting with p53DINP1 was shown to phosphorylate Ser46 of p53 [22].

Regulatory relationships of TP53INP1

• CREB and NF-kappaB Transcription Factors Regulate Sensitivity to Excitotoxic and Oxidative Stress Induced Neuronal Cell Death [31].

Other interactions of TP53INP1

• METHODS: TP53INP1 and p53 expression were examined using immunohistochemistry in 142 cases of gastric cancer [1].
• Stress-induced regulation of eukaryotic elongation factor 2 kinase by SB 203580-sensitive and -insensitive pathways [32].
• Stress-induced hypertensive rats exhibited an increased RAMP3 mRNA expression in the hypothalamus and pituitary gland (P<0.01 and P<0.05, respectively) and a decrease in the adrenal gland and midbrain (P<0.05) [33].
• Stress-induced activation of the hypothalamic-pituitary-adrenal axis would increase hypothalamic secretion of CRH [34].
• Stress-induced release of HSC70 from human tumors [35].

Analytical, diagnostic and therapeutic context of TP53INP1

• Stress-induced premature senescence in mononuclear cells from patients on long-term hemodialysis [36].
• Stress-induced analgesia: adaptive pain suppression [37].
• Stress-induced myocardial ischemia decreased concurrently, indicating improvement of myocardial perfusion [38].
• Stress-induced abnormalities of regional left ventricular wall motion were assessed by cardiokymography (CKG) during the course of maximal treadmill exercise tests in 157 patients, of whom 122 subsequently underwent coronary angiography [39].
• Stress-induced regional wall motion abnormalities developed in 91% of patients; this was not different on exercise (89%) or dobutamine echocardiography (94%) [40].

References