Disease relevance of CP1

• Group 2 latent autoimmune diabetes mellitus in adults (LADA) was defined by a minimum 6-month-long phase after diagnosis without insulin therapy, and was characterized by CP more than 200 pmol/L and anti-GAD more than 50 ng/mL (n = 70) [1].
• One of these CCAAT-binding proteins, CP1, binds with high affinity to CCAAT elements present in the human alpha-globin promoter and the adenovirus major late promoter (MLP) [2].
• Four distinct factors in extracts from murine erythroleukemia (MEL) cells interacted with the human beta-globin gene promoter CAAT box: CP1, GATA-1, and two novel factors, denoted a and b, one of which is highly inducible in the MEL system [3].
• Fibrosis was significantly induced in the EP3 rats versus EP1, CP1, and CP3 by histology, hydroxyproline content, and mRNA expression for collagen alpha1(1) and procollagen alpha2(1) [4].
• In the promoter region, we identified a CCAAT box-binding protein (CBP) that has the same binding characteristics as the CCAAT box-binding protein that binds to the Moloney murine sarcoma virus promoter and most likely represents the CP1 factor [5].

Psychiatry related information on CP1

• The recent period was remarkable for the revision of important psychological tests, including the MMPI, CPI, and MCMI, and for the emergence of new inventories, including the BPI and the ISI [6].
• The test-retest correlations were r = .48 (need for affiliation) and .56 (need for intimacy), or approximately the same as those for, e.g., the MMPI, 16PF, and CPI, It was demonstrated that this high stability over time was not due to subjects' recalling and repeating previous responses [7].
• Independent CPI masculinity and femininity scales: psychological correlates and a sex-role typology [8].
• Quadratic, inverted-U relationships were hypothesized for the self-disclosure and CPI scales, but by and large they were not found [9].
• Participants also completed the CPI and MMPI personality inventories [10].

High impact information on CP1

• This serum-induced CCAAT factor also bound CCAAT sequences from other promoters, for example, those of human heat shock protein 70, human c-Ha-ras, and human histone 1, but not to the adenovirus origin of replication or the SV40 enhancer core sequence, suggesting that it was related to CP1 or CP2 [11].
• While the point mutation in Greek HPFH slightly strengthens the binding of CP1 and the CCAAT displacement protein, the same base change strongly reduces the binding of NF-E to the distal CCAAT region, suggesting a possible role of NF-E in the repression of gamma-globin genes in adult erythroid cells [12].
• More importantly, two genes, Os CP1 and Os c6, encoding a Cys protease and a protease inhibitor, respectively, were shown to be the likely direct targets of TDR through chromatin immunoprecipitation analyses and the electrophoretic mobility shift assay [13].
• Morning peak in ventricular tachyarrhythmias detected by time of implantable cardioverter/defibrillator therapy. The CPI Investigators [14].
• METHODS AND RESULTS: Data were reviewed from 32 consecutive patients with coronary artery disease and sustained VT who had received the Ventak PRX (CPI, Inc) cardioverter-defibrillator between May 1991 and August 1993 and had experienced at least one episode of VT terminated by their device [15].

Chemical compound and disease context of CP1

• One hundred and thirty-one patients were transplanted for AML-CR1, ALL-CR1 or CML-CP1 after conditioning with 120 mg/kg body weight cyclophosphamide and 2 x 4.5 Gy TBI [16].
• Decreased CP-1 (NF-Y) activity results in transcriptional down-regulation of topoisomerase IIalpha in a doxorubicin-resistant variant of human multiple myeloma RPMI 8226 [17].
• We investigated the effect of two types of carnitine palmitoyltransferase I inhibitors, ethyl 2-(6-(4-chlorophenoxy)hexyl)oxirane-2-carboxylate (etomoxir) and (R)-3-carboxy-N,N, N-trimethyl-2-¿[hydroxy(tetradecyloxy)phosphinyl]oxy¿-1-propana minium hydroxide (SDZ CPI 975), on cardiac and hepatic hypertrophy in ddY mice [18].
• To assess their relevance in the progression of non-small cell lung cancer (NSCLC) the protein level, cysteine protease activity (CPI) and localization of type I (stefins A and B) and type II (C, E/M and F) cystatins were defined in tumours and control lung counterparts from 165 patients [19].
• Thinning of the epidermis and telangiectasia were noted 3 weeks after application of betamethasone-17-valerate (BV), budesonide (BD), clobetasol-17-propionate (CP), and fluocinolone acetonide (FA), but not of hydrocortisone (HC) [20].

Biological context of CP1

• Of interest, these two amino acids are also found in the homologous positions of CP 9 and 16, which form part of the C3b binding site of Hu CR1 [21].
• Its cDNA-derived amino acid sequence contains complement protein-repeating modules (CP) 1-6, 28, 29, and 30 in tandem and is 98.8% homologous to the corresponding regions of human (Hu) CR1 [21].
• In our study, we investigated the relationship of HLA class II alleles to antibody production against glutamic acid decarboxylase (GADab) and to C-peptide secretion (CP) in diabetic patients [22].
• Our results show that the structure of this promoter only permits productive interactions of the two transcription factors Sp1 and CP1 with the basal transcription machinery in the presence of enhancer sequences [23].
• Activation transcription factor (ATF) and CP1 showed dramatically different interactions with the factor(s) bound to the TATA region [24].

Anatomical context of CP1

• Two murine mAb were prepared against human mast cell carboxypeptidase (HMC-CP) purified from human skin, and were termed CP1 and CP2, respectively [25].
• An overlapping binding site for the CCAAT box-binding factor CP1 is required for derepressed promoter activity in HeLa and K562 cells, but is dispensable in HEL cells, indicating that different cell types require distinct cis-elements for gp91(phox) promoter activity [26].
• Immunohistochemical labeling of peripheral blood leukocytes resulted in staining of monocytes with CP2 but not with CP1 [25].
• These results demonstrate the importance of cell concentration and treatment conditions for maximizing the depletion of BM T cells with CP1 + C' [27].
• Mean recoveries of CFU-GM (day 7), CFU-GM (day 14), CFU-GEMM, and BFU-E growth following CP1 + C' were 51, 43, 42, and 45% respectively [27].

Associations of CP1 with chemical compounds

• It differs from the C4b binding site of Hu CR1 only by two amino acids, Tyr for Ser37 in CP 1 and Asp for Gly79 in CP 2 [21].
• The role of nuclear factor NF-Y/CP1 in the transcriptional regulation of the human aldehyde dehydrogenase 2-encoding gene [28].
• Ten ICA positive cases studied were showing non-significant C-peptide (CP) release (after glucose load) in comparison to negative cases (14); p < 0.05, 8 of these cases were with < 3 months duration [29].
• Finally, although CP1 caused the formation of massive aggregates, as did D10, there was little turbidity change with the depsipeptide as opposed to the peptide [30].
• The antimitotic depsipeptide cryptophycin 1 (CP1) was compared to the antimitotic peptide dolastatin 10 (D10) as an antiproliferative agent and in its interactions with purified tubulin [30].

Physical interactions of CP1

• Thus, the proximal ALDH2 promoter was bound by NF-Y/CP1 and this transcription factor may be responsible for the basal expression of the gene observed in most tissues [28].
• The reduction in expression is relieved when the CDP/CP1-binding site is removed from the gp91-phox promoter, confirming that it is a target for repression [31].

Regulatory relationships of CP1

• In conjunction with previous mutation analyses, these results suggest that C/EBPgamma may collaborate with CP1 to enhance transcription through the beta-globin CAAT box [32].

Other interactions of CP1

• HuR and CP1 bound simultaneously to the UC-rich RNA and in a cooperative manner [33].
• The heat stability, resistance to proteinase K digestion, sensitivity to inhibition of DNA binding by o-phenanthroline, and immunological properties of the liver factor binding to FP160 were very similar to the corresponding properties of NF-Y/CP1 [28].
• Furthermore, using a method that combines UV cross-linking and immunoprecipitation, we show that antibodies specific to ATF-2 are able to specifically precipitate protein-protein-DNA complexes containing NF-I and CP1 [34].
• The CCAAT-binding factor NF-Y (CBF/CP1) is a heteromeric transcription factor involved in the regulation of a variety of eukaryotic genes [35].
• CP and CP1 preparations equally inhibit this reaction [36].

Analytical, diagnostic and therapeutic context of CP1

• DNase I and gel mobility shift assays show the binding of a number of nuclear factors to these elements, including Sp1 and CP1 [23].
• Immunoprecipitation studies confirmed that HuR and CP1 associate with p21(WAF1) mRNA in MDA-468 cells [37].
• TETR-PCR for C. pneumoniae with primer set CPN 90-CPN 91 was 90% sensitive and 93.3% specific compared with a nested PCR with primer set CP1/2-CPC/D for clinical respiratory samples [38].
• A fluorescently labeled DNA probe designed from the CP1 sequence was used for in situ hybridization experiments to verify that the sequence obtained was derived from the observed Cristispira cells [39].
• After balloon angioplasty, the number and the mean diameter of particles increased with CP1, CP2, and CP3 [40].

References