Disease relevance of SELENBP1

• We have also successfully expressed hSP56 in Escherichia coli using the expression vector-pAED4 [1].
• Here I showed that selenium-binding protein (SBP) was exclusively located at the leading edges of rapidly growing protrusions in newly plated T98G glioma cells, and at the growing tips of the neurites in SH-SY5Y neuroblastoma cells [2].
• SELENBP1 expression was reduced in 87% cases of invasive ovarian cancer (122/141) and was significantly reduced in borderline tumors and invasive cancers (p<0.001) [3].
• Our findings indicate that suppression of SELENBP1 is a frequent and late event in colorectal carcinogenesis, and may contribute to the rapid progression of colorectal carcinoma [4].
• Among them, selenium-binding protein 1 (SELENBP1) was markedly decreased in 12 (85%) carcinomas [4].
• SELENBP1 expression decreased significantly in Barrett's esophagus to adenocarcinoma progression [5].

Psychiatry related information on SELENBP1

• RESULTS: Systolic BP (SBP) was linearly related significantly to BMI and alcohol consumption, whereas diastolic BP (DBP) was related to age [6].
• Physical activity had a positive effect on SBP [7].

High impact information on SELENBP1

• Furthermore, the Cnr phenotype results from a spontaneous epigenetic change in the SBP-box promoter [8].
• Using positional cloning and virus-induced gene silencing, here we demonstrate that an SBP-box (SQUAMOSA promoter binding protein-like) gene resides at the Cnr locus [8].
• Comparative gene expression analysis of blood and brain provides concurrent validation of SELENBP1 up-regulation in schizophrenia [9].
• According to our model, 12 amino acid residues lining the Arabidopsis 4CL isoform 2 (At4CL2) substrate binding pocket (SBP) function as a signature motif generally determining 4CL substrate specificity [10].
• Differential expression and androgen regulation of the human selenium-binding protein gene hSP56 in prostate cancer cells [11].

Chemical compound and disease context of SELENBP1

• Interestingly, SELENBP1 mRNA and protein levels were reduced by androgen and elevated by selenium treatment in the normal HOSE cells, whereas reversed responses were observed in the ovarian cancer cell lines [3].
• After 50 weeks of therapy with delapril/manidipine 30mg/10mg once daily, mean SBP/DBP was reduced by 22/14mm Hg in patients with mild to moderate hypertension (n = 309) [12].

Biological context of SELENBP1

• The hSP56 gene is located at human chromosome 1q21-22) [1].
• However, systolic BP (SBP) variability also may be induced by fluctuations in stroke volume through left ventricular end-diastolic pressure (LVEDP) variability via dynamic ventricular-arterial coupling during respiration [13].
• Seven healthy young subjects underwent 6-min recordings of beat-by-beat LVEDP, SBP, and HR in the supine position with controlled respiration at 0.2 Hz during hyper- and hypovolemia [13].
• Dynamic ventricular-arterial coupling gain (Gain LVEDP-SBP) was smaller by 25% (P = 0.009) during hypervolemia than during hypovolemia, whereas arterial-cardiac baroreflex function gain (Gain SBP-HR) was similar [13].
• To assess whether a decrease in SBP (systolic blood pressure) or a change in metabolic control would improve the long-axis function, 48 Type II diabetic patients participating in the CALM II (Candesartan and Lisinopril Microalbuminuria II) study were included in the present study [14].

Anatomical context of SELENBP1

• The results indicate that the membrane of the myeloma cell line SP56 is more suitable for use in the TBII assay than the porcine thyroid membrane, in terms of sensitivity to autoantibodies against TSHR in human sera [15].
• There were no differences in carotid sinus SBP between PPM-C and PPM-NP during -Gr [16].
• INTRODUCTION: The push-pull maneuver (PPM) is defined as a reduction in G-tolerance when positive acceleration (+Gz) immediately follows negative acceleration (-Gz) exposure, with the carotid baroreceptors presumably playing a dominant role in the ensuing BP (SBP) responses [16].
• Tet lowered SBP, left ventricular weight to body weight ratio, vascular media thickness, media to lumen ratio, cardiac and vascular wet weight, and collagen content [17].
• Selenium-binding protein-1 in smooth muscle cells is downregulated in a rhesus monkey model of chronic allograft nephropathy [18].

Associations of SELENBP1 with chemical compounds

• Selenium can disrupt the androgen pathway, which has been implicated in modulating SELENBP1 expression [3].
• In experiments with SBP (6-135 nM), the concentrations of unbound testosterone in the superfusion medium were reduced to the same levels as in the experiments with HSA [19].
• During the 24-hour period, brimonidine induced a significant decrease in systolic BP (SBP) and DBP at all time points when compared with baseline measurements and with those after administration of the other drugs (P<0.0001) [20].
• Timolol caused a significant decrease in DBP and SBP at all the 24-hour time points when compared with the baseline and with the dorzolamide- and latanoprost-induced changes (P<0.0001) [20].
• In nonresponders to monotherapy with delapril (n = 155) or manidipine (n = 152), delapril/manidipine 30mg/10mg once daily for 12 weeks reduced mean SBP/DBP by 16/11mm Hg and 16/10mm Hg, respectively [12].

Other interactions of SELENBP1

• The protein expression status of human selenium-binding protein 1 (SBP1) in human tumours and the exact function of this protein are not known [21].
• Diverse regulations also occurred with proteins involved in cell proliferation and differentiation, such as GMP reductase 2 and creatine kinase B, and proteins bearing potential tumor suppressor activities, including prohibitin and selenium binding protein 1 [22].

Analytical, diagnostic and therapeutic context of SELENBP1

• The reduced expression of SELENBP1 was further supported by Western blot analysis and immunohistochemistry [4].
• Suppression of SELENBP1 was further analyzed in another eight-paired adenomas and carcinomas from the same patients using Western blot analysis and immunohistochemistry, and revealed that one adenoma and seven carcinomas exhibited markedly reduced SELENBP1 expression [4].
• Patients with low levels of SELENBP1 expression had significantly lower overall survival rates (72 vs. 85%, p = 0.021) among the 240 stages II and III colorectal carcinomas by using tissue microarray analysis [4].
• It also reviews the current knowledge and applications to date of SBP, particularly biosensors [23].
• Both SBP and DBP were adjusted for the effects of body mass index (BMI) using regression procedures [24].

References