Disease relevance of LOC396767

• Modulation of p53 cellular function and cell death by African swine fever virus [1].
• Proteins p93-96, p69, p53, p47 and p13 corresponded by their mol wt to proteins NV5, NV4, V3 and V2 (NV1 1/2) of mosquito-borne flaviviruses [2].

High impact information on LOC396767

• At the stages of tissue regeneration, these mechanisms include both the expression of growth factors that promote cell proliferation and the suppression of p53 that downregulates proliferation [3].
• Differentiation was characterized by down-regulation of CD14, MHC Ags, the monocytic SWC1 marker, and p53; concomitant up-regulation of the SWC9 macrophage marker, a putative porcine CD80 (detected with anti-human CD80 Ab), and acid phosphatase secretion were also characteristic [4].
• Male Sprague-Dawley rats underwent bilateral renal artery clamp for 30 min followed by reperfusion. p53 protein levels increased significantly in the medulla over 24 h post-ischemia [5].
• Induction of SMC apoptosis by transient p53 overexpression positively influenced vein graft remodeling [6].
• We have studied the function of p53 in African swine fever virus (ASFV) infection by determining the expression and activity of this transcription factor in infected cells. p53 levels are increased at early times of infection and are maintained throughout the infectious cycle [1].

Biological context of LOC396767

• The protein is transcriptionally active, stabilized by phosphorylation, and localized in the nucleus. p53 induces the expression of p21 and Mdm2 [1].
• It is possible that trans-activating p21 may mediate the halting of the cell cycle through the CsA-induced accumulation of p53 [7].
• The down-regulation of the porcine monocyte marker SWC1, and up-regulation of the SWC9 macrophage marker were retarded, but not inhibited, as was the differentiation-associated down-regulation of p53 and myeloperoxidase [8].
• In conclusion, the density of 5 x 10(6) cells/ml is a critical inflection point for most of the functional parameters, although p53 gene expression is not elevated at this cell density [9].
• Expression of oncogenes c-myc and p53 was induced, and except for caspase 1, all the other caspases tested were activated [10].

Anatomical context of LOC396767

• The mass of hepatocytes in each device was evaluated for (a) cell viability, (b) ability to degrade diazepam, (c) ability to synthesize urea, (d) incorporation of [3H]-leucine into protein, (e) glucose-6-phosphatase activity, (f) total RNA content, and (g) p53 gene expression [9].
• S-(1,2-dichlorovinyl)-L-cysteine-induced dedifferentiation and p53 gene mutations in LLC-PK1 cells: a comparative investigation with S-(2-chloroethyl)cysteine, potassium bromate, cis-platinum and styrene oxide [11].
• In conclusion, our results demonstrate that early mVSMC migration from the tunica media requires mitogen-induced suppression of p53 that is highly expressed in contractile mVSMCs residing in the healthy vessel wall [12].
• Mitogen-induced p53 downregulation precedes vascular smooth muscle cell migration from healthy tunica media and proliferation [12].
• PCNA, Bcl-2, p53, and p21 in noise-exposed and non-noise-exposed guinea pig cochleas are not affected by exogenous FGF-1 [13].

Associations of LOC396767 with chemical compounds

• In this study we investigated by polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP) analysis and direct sequencing if S-(1,2-dichlorovinyl)-L-cysteine-induced LLC-PK1 clones display mutations in the p53 gene in comparison with wild-type clones [11].
• On the other hand, N-acetylcysteine prevented cisplatin-induced apoptosis as well as c-myc induction but not p53 induction [10].
• These clones displayed also band shifts of p53 exon 7, indicating mutations, which were confirmed by sequencing: a double mutation consisting of a base substitution followed by one base insertion in the case of S-(1,2-dichlorovinyl)-L-cysteine and potassium bromate and a base substitution in the case of cis-platinum [11].

Other interactions of LOC396767

• Serum deprivation-induced apoptosis in cultured porcine granulosa cells is characterized by increased expression of p53 protein, Fas antigen and Fas ligand and by decreased expression of PCNA [14].

Analytical, diagnostic and therapeutic context of LOC396767

• The formation of sunburn cells was confirmed by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) method. p53-positive cells, and p21-positive cells appeared at 6 h, and 12 h, respectively, following the UVB-irradiation [15].
• Immunohistochemistry was used to demonstrate the presence of p53 protein [16].

References