共查询到20条相似文献,搜索用时 31 毫秒
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Y Tanaka H F DeLuca A Akaiwa M Morisaki N Ikekawa 《Archives of biochemistry and biophysics》1976,177(2):615-621
An epimeric mixture of 24-hydroxy-[24-3H]vitamin D3 was synthesized by the reduction of 24-ketovitamin D3 by sodium borotritide. The epimeric mixture was converted to the trimethylsilylether derivatives and subjected to high-pressure liquid chromatography using silica gel columns to separate the 24-hydroxy-[24-3H]vitamin D3 isomers. The 24R-hydroxy-[24-3H] vitamin D3 induced calcification in rachitic rats while the 24S-hydroxy-[24-3H] vitamin D3 had little or no such activity. As both isomers of 24-hydroxy-vitamin D3 are metabolized to 24,25-dihydroxyvitamin D3, it appears that the 24-hydroxyvitamin D3-25-hydroxylase does not discriminate between the isomers. Only the R-isomer of 24-hydroxyvitamin D3 is metabolized to 1,24-dihydroxyvitamin D3, although only trace amounts of this compound were found 2 days after the administration of 24-hydroxyvitamin D3. The striking difference in the metabolism of the isomers is the high selectivity of the 1-hydroxylase for R-isomer. It is suggested that the high specificity of biological activity for the R-isomer of 24-hydroxyvitamin D3 is because of the specificity of the 1-hydroxylation of 24,25-dihydroxyvitamin D3 for the R configuration. 相似文献
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D22S15--a fetal brain cDNA with BanII and SacI RFLP. 总被引:2,自引:0,他引:2
G A Rouleau D M Kurnit R L Neve A Bazanowsky D Patterson J F Gusella 《Nucleic acids research》1988,16(4):1646
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Wim Van Hul Hubert Backhovens Guy Van Camp Piet Stinissen Marc Cruts Anita Wehnert Christine Van Broeckhoven 《Human genetics》1991,87(2):109-111
Summary We were able to refine the chromosomal position of two existing marker loci, using an extended chromosome 21 somatic cell hybrid panel. The locus D21S26 mapped in the region 21q11.2–q21.1, and the locus D21S24 in 21q22.1–q22.2. Physical and genetic analysis indicated that D21S26 is tightly linked to D21S13 and D21S16, two markers previously linked to familial Alzheimer's disease. 相似文献
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rig encodes ribosomal protein S15. The primary structure of mammalian ribosomal protein S15 总被引:4,自引:0,他引:4
M Kitagawa S Takasawa N Kikuchi T Itoh H Teraoka H Yamamoto H Okamoto 《FEBS letters》1991,283(2):210-214
rig, a gene originally isolated from a rat insulinoma cDNA library, codes for a basic 145 amino acid protein [( 1986) Diabetes 35, 1178-1180]. Here we show that the immunoreactivity to a monoclonal antibody against the deduced rig protein and the translation product of rig mRNA comigrated with ribosomal protein S15. The amino acid sequence of ribosomal protein S15 purified from rat liver coincided with that deduced from the nucleotide sequence of rig mRNA, but there were indications that the initiator methionine was removed and the succeeding alanyl residue was monoacetylated. From these results, we conclude that the product of rig is ribosomal protein S15. 相似文献
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Yuanhua Cheng Steffen Lindert Peter Kekenes-Huskey Vijay?S. Rao R.?John Solaro Paul?R. Rosevear Rommie Amaro Andrew?D. McCulloch J.?Andrew McCammon Michael Regnier 《Biophysical journal》2014,107(7):1675-1685
During β-adrenergic stimulation, cardiac troponin I (cTnI) is phosphorylated by protein kinase A (PKA) at sites S23/S24, located at the N-terminus of cTnI. This phosphorylation has been shown to decrease KCa and pCa50, and weaken the cTnC-cTnI (C-I) interaction. We recently reported that phosphorylation results in an increase in the rate of early, slow phase of relaxation (kREL,slow) and a decrease in its duration (tREL,slow), which speeds up the overall relaxation. However, as the N-terminus of cTnI (residues 1–40) has not been resolved in the whole cardiac troponin (cTn) structure, little is known about the molecular-level behavior within the whole cTn complex upon phosphorylation of the S23/S24 residues of cTnI that results in these changes in function. In this study, we built up the cTn complex structure (including residues cTnC 1–161, cTnI 1–172, and cTnT 236–285) with the N-terminus of cTnI. We performed molecular-dynamics (MD) simulations to elucidate the structural basis of PKA phosphorylation-induced changes in cTn structure and Ca2+ binding. We found that introducing two phosphomimic mutations into sites S23/S24 had no significant effect on the coordinating residues of Ca2+ binding site II. However, the overall fluctuation of cTn was increased and the C-I interaction was altered relative to the wild-type model. The most significant changes involved interactions with the N-terminus of cTnI. Interestingly, the phosphomimic mutations led to the formation of intrasubunit interactions between the N-terminus and the inhibitory peptide of cTnI. This may result in altered interactions with cTnC and could explain the increased rate and decreased duration of slow-phase relaxation seen in myofibrils. 相似文献
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Yuanhua Cheng Steffen Lindert Peter Kekenes-Huskey Vijay S. Rao R. John Solaro Paul R. Rosevear Rommie Amaro Andrew D. McCulloch J. Andrew McCammon Michael Regnier 《Biophysical journal》2014
During β-adrenergic stimulation, cardiac troponin I (cTnI) is phosphorylated by protein kinase A (PKA) at sites S23/S24, located at the N-terminus of cTnI. This phosphorylation has been shown to decrease KCa and pCa50, and weaken the cTnC-cTnI (C-I) interaction. We recently reported that phosphorylation results in an increase in the rate of early, slow phase of relaxation (kREL,slow) and a decrease in its duration (tREL,slow), which speeds up the overall relaxation. However, as the N-terminus of cTnI (residues 1–40) has not been resolved in the whole cardiac troponin (cTn) structure, little is known about the molecular-level behavior within the whole cTn complex upon phosphorylation of the S23/S24 residues of cTnI that results in these changes in function. In this study, we built up the cTn complex structure (including residues cTnC 1–161, cTnI 1–172, and cTnT 236–285) with the N-terminus of cTnI. We performed molecular-dynamics (MD) simulations to elucidate the structural basis of PKA phosphorylation-induced changes in cTn structure and Ca2+ binding. We found that introducing two phosphomimic mutations into sites S23/S24 had no significant effect on the coordinating residues of Ca2+ binding site II. However, the overall fluctuation of cTn was increased and the C-I interaction was altered relative to the wild-type model. The most significant changes involved interactions with the N-terminus of cTnI. Interestingly, the phosphomimic mutations led to the formation of intrasubunit interactions between the N-terminus and the inhibitory peptide of cTnI. This may result in altered interactions with cTnC and could explain the increased rate and decreased duration of slow-phase relaxation seen in myofibrils. 相似文献
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P H Stern H F DeLuca N Ikekawa 《Biochemical and biophysical research communications》1975,67(3):965-971
R and S isomers of 24-OH-D3 and 24,25-(OH)2D3 were tested for their effects on bone resorption . 24(R), 25-(OH)2D3 was more active than 24(S),25-(OH)2D3. Likewise, 24(R)-OH-D3 was more active than 24(S)-OH-D3. The bone resorbing activity of 24(R)-OH-D3 was equivalent to that of 25-OH-D3; 24(R),25-(OH)2D3 was somewhat less potent. The results indicate that there is discrimination between the isomers of these compounds at the level of the responding tissue. 相似文献
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The human lysyl oxidase-like gene maps between STS markers D15S215 and GHLC.GCT7C09 on chromosome 15
The lysyl oxidase-like (LOXL) gene is a new member of the lysyl oxidase family, a copper-dependent enzyme that is implicated
in the crosslinking of collagen and elastin fibers. We have mapped the LOXL gene to chromosome 15q23, between STS markers
D15S215 and GHLC.GCT7C09. This position corresponds to the q23 locus, not to the q24-25 locus suggested in a preliminary report.
Received: 16 July 1997 / Accepted: 30 July 1997 相似文献
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