Disease relevance of CHP

• The purified CHP and rat DRAK2 proteins synthesized in Escherichia coli could bind in vitro [1].
• For each of two human neuroblastoma cell lines (CHP 100 and CHP 126), exposure to each drug individually produced dose-related cytotoxic effects within 3 days [2].
• CHP was essentially equipotent, however, with cortisol in models of inflammation mediated via delayed hypersensitivity such as experimental allergic encephalomyelitis, adjuvant-induced arthritis, mouse skin graft, and mouse skin delayed hypersensitivity [3].
• 6-Chloro-17 alpha-hydroxypregna-1,4,6-triene-3,20-dione (CHP), a steroid having a progestin-type structure yet not having progestational activity, was found to exhibit moderate anti-inflammatory activity in a number of conventional tests for corticoid potency (e.g., thymolytic, granuloma, carrageenin edema) [3].
• We conclude that this focal complication suggests a continuum between dermatomyositis, CHP, and IMAM, the three syndromes where T-cell activation plays an important role [4].

Psychiatry related information on CHP

• Furthermore, administration of exogenous CHP to C57BL mice caused a pronounced decrease in their voluntary alcohol consumption [5].

High impact information on CHP

• These findings suggest that CHP serves as an obligatory subunit that is required both for supporting the basic activity and regulating the pH-sensing of NHE1 via interactions between distinct parts of these proteins [6].
• The plasma membrane Na+/H+ exchangers (NHE) require calcineurin B homologous protein (CHP) as an obligatory binding partner for ion transport [6].
• Structure-based mutagenesis revealed the importance of hydrophobic interactions between CHP/NHE1 for the function of NHE1 [6].
• The phosphorylation state of CHP may therefore be an important signal controlling mitogenic regulation of NHE1 [7].
• To explore this possibility, we studied the effects of desferoxamine, a compound which chelates iron, on viability of CHP 126 and CHP 100, two human neuroblastoma cell lines [8].

Chemical compound and disease context of CHP

• In order to understand control mechanisms for the biosynthesis of these fucosylated glycoconjugates, GDP-L-Fuc-N-acetyl-beta-D-glucosaminide alpha 1----3fucosyltransferase was purified from human neuroblastoma cells, CHP 134, utilizing either the immobilized oligosaccharide or disaccharide substrates [9].
• Proliferation of neuroblastoma cells (SK-N-MC and CHP 234) was evaluated by 5-bromo-2'-deoxyuridine incorporation during DNA synthesis in vitro [10].
• Here we report the analysis of human AMPA and kainate receptor expression in four neuroblastoma cell lines (SK-N-MC, IMR-32, CHP 126 and NMB/N7) [11].
• To further understand the mechanism of deferoxamine-induced cytotoxicity, we looked at its effects on cell cycling and on DNA, RNA, and protein synthesis by CHP 126, a cell line that is derived from tumor tissue of a patient with a neuroblastoma and that is known to be drug sensitive [12].
• A fast protein liquid chromatography (FPLC) method for study of thyrotropin-releasing hormone (TRH) and its metabolite histidyl-proline diketopiperazine (CHP) in human blood: degradation in liver and pancreatic diseases [13].

Biological context of CHP

• Ubiquitous calcineurin B homologous protein (CHP or p22) is co-localized and co-immunoprecipitated with expressed NHE1, NHE2, or NHE3 independently of its myristoylation and Ca2+ binding, and its binding site was identified as the juxtamembrane region within the carboxyl-terminal cytoplasmic domain of exchangers [14].
• We have cloned a new rat CHP isoform (rCHP2) and characterized the binding property to NHEs and the tissue distribution. rCHP2 binds to the juxtamembrane region of plasma membrane-type NHE isoforms (NHE1-5) in vivo and in vitro as well as rCHP1 (original rat CHP) [15].
• This substrate specificity correlates with the oligosaccharide residues thus far defined on glycoproteins of CHP 134 cells since NeuAc and Fuc alpha 1----3GlcNAc have yet to be detected on the same oligosaccharide antenna [9].
• The relationship between the quantity of silver-stained interphasic nucleolar organizer regions (NORs) and nuclear synthetic activity, caryotype, and growth rate was studied in two established neuroblastoma cell lines (CHP 212 and HTB 10) [16].
• In contrast to cortisol, which inhibits both 19-s and 7-s antibody formation, CHP does not diminish the number of cells producing either antibody [3].

Anatomical context of CHP

• Calcineurin homologous protein (CHP) is a Ca2+-binding protein that directly interacts with and regulates the activity of all plasma-membrane Na+/H+-exchanger (NHE) family members [17].
• Moreover, prolonged activation of Jurkat cells was associated with a decreased abundance of CHP, suggesting a possible regulatory mechanism allowing activation of calcineurin [18].
• In Jurkat and HeLa cells, overexpression of CHP specifically impaired the nuclear translocation and transcriptional activity of NFAT but had no effect on AP-1 transcriptional activity and only a small (<25%) inhibitory effect on the transcriptional activity of NFkappaB [18].
• KIF1Bbeta2, capable of interacting with CHP, is localized to synaptic vesicles [19].
• These results suggest that CHP2 functions in the absorptive epithelium for the intestine with NHE(s) [15].

Associations of CHP with chemical compounds

• Lesser interindividual variations were observed with respect to human liver GST activities towards benzo(a)pyrene-4,5-oxide (BaPO, 9-fold variation), 1-chloro-2,4-dinitrobenzene (CDNB, 8.5-fold variation), cumene hydroperoxide (CHP, 5-fold variation), and p-nitrophenyl acetate (NPA, 4-fold variation) [20].
• In this study, we used biocompatible nanogels composed of a polysaccharide pullulan backbone with hydrophobic cholesterol moieties (cholesterol-bearing pullulan, CHP) as artificial chaperones to inhibit the formation of Abeta-(1-42) fibrils with marked amyloidgenic activity and cytotoxicity [21].
• In particular, the irreversible aggregation of carbonic anhydrase B (CAB) upon heating was completely prevented by complexation between the heat-denatured enzyme and hydrogel nanoparticles formed by the self-aggregation of cholesteryl group-bearing pullulan (CHP) [22].
• However, line CHP 100 proved hypersensitive to amsacrine, bleomycin, methotrexate and vincristine yet refractory to cisplatin, carboplatin and VP-16, compared with the other two lines [23].
• The first step was also activated the surface of CHP to induce primary amine terminator [24].

Physical interactions of CHP

• Crystallization and preliminary crystallographic analysis of the human calcineurin homologous protein CHP2 bound to the cytoplasmic region of the Na+/H+ exchanger NHE1 [17].
• CHP binds to regions adjacent to the motor domains of KIF1Bbeta2 and KIF1B, but not to those of the other KIF1 family members, KIF1A and KIF1C [19].

Regulatory relationships of CHP

• In conclusion, SK-N-MC cells which grow rapidly and have a high plating efficiency, express IGF-I, while CHP cells that grow more slowly express IGF-II [25].

Other interactions of CHP

• In this study, we characterized the function of another isoform of CHP (designated CHP2) that has a 61% amino acid identity with CHP1 [26].
• IGFBP-2 secretion correlated positively with IGF-II secretion in CHP cells (r=0.85, P=0.05) and negatively with IGF-I (r= -0.9, P<0.01) in SK-N-MC cells [25].
• The results of this study show that the level of CHP, a peptide that mimics dopamine in many of its pharmacologic actions, is lower in brains of alcohol-preferring C57BL mice compared to alcohol non-preferring DBA2 mice [5].
• Neither CoQ10 nor vitamin E correlated with paraoxonase (PON) activity or cholesteryl-ester hydroperoxides (CHP) [27].
• CONCLUSIONS: These findings indicate that CHP/ESO is a promising polyvalent cancer vaccine targeting NY-ESO-1 [28].

Analytical, diagnostic and therapeutic context of CHP

• In situ hybridization experiments demonstrated the abundant expression of CHP2 in the epithelial cell layer of villi of the small intestine in contrast with the expression of CHP1 in both the epithelial layer and connective tissues [15].
• Only 30% of the cells in the line CHP 100 bound MI/N1 as determined by indirect immunofluorescence [29].
• The linkage between CHP and HMDI will be characterized by FTIR [24].
• In contrast, only 66% of cells in the fourth neuronal line (CHP 100) were Thy-1+, although these showed strong immunofluorescence [30].
• CHP-LI was detected in all AF samples and was indistinguishable from synthetic CHP by immunoidentity, by gel chromatography on Sephadex G-25, and by high pressure liquid chromatography [31].

References