Disease relevance of BP1

• Correspondingly, women with BP1 levels higher than 39 ng/ml had an odds ratio of 0.21 (95% CI, 0.07-0.68) for breast cancer [1].
• Multivariate regression analysis that controlled for maternal height, prepregnancy weight, smoking behavior, infant gender, gestational age, parity, as well as amniocentesis week showed that higher AF IGF BP1 was associated with lower birth weight (partial r2 = 0.0062) [2].
• We present here a novel observation of an approximately 253-kb deletion between BP1 and BP2 on 15q11.2, in a 3(1/2)-year-old boy, who was referred to us with a clinical suspicion of having Angelman syndrome and presenting with mental retardation, neurological disorder, developmental delay and speech impairment [3].
• This BP is immunologically distinct from the low molecular weight fetal rat BP (rBP2) and is related to the human amniotic fluid BP (hBP1) that is increased in patients with insulin dependent diabetes mellitus [4].
• The blood pressure QTL 1a and QTL 1b defined here overlap significantly with QTL for disease phenotypes of renal failure, stroke, ventricular mass, and salt susceptibility defined in other rat strains, implying that these disease phenotypes and our blood pressure phenotype have causes in common [5].

High impact information on BP1

• Three independent clonal lines were obtained that secreted IgG HumAbs, including one IgG1 kappa (BP3) and two distinct IgG4 kappa (BP1 and BP2) [6].
• Thus, the blood pressure QTL on Chr 1 is located centromeric to the Sa gene locus in a region that is syntenic to human chromosome 11p15.4-p15 [7].
• The data from two congenic strains combined unequivocally establish the existence of a blood pressure QTL on rat chromosome 2 [8].
• The main myelin proteins consisted of (1) two basic proteins, BPa and BPb (11,500 and 13,000 MW, similar to those of trout central nervous system (CNS) myelin proteins BP1 and BP2), and (2) two glycosylated components, IPb (24,400 MW) and IPc (26,200 MW) [9].
• Of the three active compounds in vivo, 3BC induced vitellogenin at lower concentrations (435 microg/l) than BP1 (4919 microg/l) and BP2 (8783 microg/l) [10].

Biological context of BP1

• These results show that 2nd trimester AF IGF BP1, BP3, and IGF II may emerge as early indicators of fetal growth [2].
• CONCLUSIONS: These data suggest that insulin strongly regulates pre- and post-translational renal IGF BP1 gene expression and implicate BP1 as an important determinant of IGF-I activity in diabetic kidney [11].
• The average maximum diameter measured for the whole colon was 5.2+/-0.6cm in prone position and 4.8+/-0.6cm in the supine position in BP1 (p<0.01) [12].
• The inhibition of translation is characterized by increased phosphorylation of the alpha subunit of eukaryotic initiation factor eIF2 and dephosphorylation of the eIF4E-binding protein 4E-BP1 [13].

Associations of BP1 with chemical compounds

• RESULTS: Rapid time- and STZ dose-dependent increases in both pre- and post-translational renal IGF BP1 expression were noted in the untreated diabetic animals [11].

Other interactions of BP1

• To our knowledge a microdeletion limited only to the BP1-BP2 region has not yet been reported [3].
• [7] Current source density maps, which were relatively robust between different tasks, further demonstrated that BP1 stemmed from the fronto-central midline (mesial wall motor areas) [14].

Analytical, diagnostic and therapeutic context of BP1

• IGF-1, BP1, and BP3 levels were determined by immunoradiometric assays [1].
• In this study, we report the further dissection of this Chr 1 blood pressure QTL with congenic substitution mapping [7].
• Transcriptional profiling with a blood pressure QTL interval-specific oligonucleotide array [15].

References