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1 ecular weight guests such as proteins (e.g., human insulin).
2 y profiles compared with that of recombinant human insulin.
3 t in birds and fish) augments the potency of human insulin.
4 gic and saturating concentrations of regular human insulin.
5 ein can be used to extend the time action of human insulin.
6 or tetraplex structures in the expression of human insulin.
7 1.35 A, is essentially identical to that of human insulin.
8 -glucose abolished the stimulatory effect of human insulin (1 nM, 8 h) on L-[3H]leucine incorporation
9 was achieved by administering a recombinant human insulin a few hours after Albulin injection in mic
10 ted transgenic potato plants that synthesize human insulin, a major insulin-dependent diabetes mellit
12 of action of [N(epsilon)-palmitoyl Lys(B29)] human insulin administered intravenously was nearly twic
16 ls is to screen the amyloid-forming proteins human insulin and beta(2)-microglobulin for segments tha
17 nstrated that the presence of high levels of human insulin and bovine insulin does not interfere with
18 n glucose stimulation of the implanted mice, human insulin and C-peptide are detected in sera at leve
19 was assessed by measuring the production of human insulin and C-peptide over a period of 3-15 months
20 In vivo function was assessed by measuring human insulin and C-peptide production, and by the abili
22 f Chinese hamster ovary cells expressing the human insulin and EGF receptors resulted in a time-depen
24 imultaneous, direct quantification of intact human insulin and five insulin analogs in human plasma.
26 glycemic control similar to that of premixed human insulin and may provide tighter glycemic control t
27 ogical efficacy, we used UTMD to deliver RIP-human insulin and RIP-hexokinase I plasmids to islets of
30 venously was nearly twice that of unmodified human insulin, and the plasma half-life was nearly seven
31 eak daf-2 mutants, suggesting that INS-1 and human insulin antagonize DAF-2 insulin-like signaling.
32 t the potency and thermodynamic stability of human insulin are enhanced in concert by substitution of
33 the C-terminal prolyl and lysyl residues of human insulin are inverted, and protamine that is used a
35 , we characterize the aggregation process of human insulin at acidic pH in the presence of sulfate io
36 ate of the protein, the crystal structure of human insulin at pH 2.1 has been determined to 1.6 A res
37 two class III VNTR constructs linked to the human insulin basal promoter or SV40 heterologous promot
38 educed three out of four disulfide bridges), human insulin, bovine core histones, and human alpha-syn
39 e investigated the fibrillation of monomeric human insulin by monitoring changes in CD, attenuated to
43 insulin/IGF-1 signaling pathway by ingested human insulin can alter NF-kappaB-dependent immunity, an
46 INS-1res cells with a plasmid containing the human insulin cDNA and expansion of the transfected colo
47 the liver-specific albumin promoter, and the human insulin cDNA modified for furin cleavage compatibi
48 Four lines of transgenic mice harboring a human insulin cDNA with expression driven by the goat be
50 ls, is processed and stored as CpepSfGFP and human insulin comprising only approximately 0.04% of tot
51 lin infusion (group 3) achieved steady-state human insulin concentrations of 22,000 plus minus 1,800
52 infusion (group 2) established steady-state human insulin concentrations of 6,300 plus minus 510 pmo
53 nstant whether in the absence or presence of human insulin concentrations sufficient to saturate the
54 is structure leads to a model for fibrils of human insulin consistent with electron microscopic, x-ra
55 trix protease Ste23 in yeast, a homologue of human insulin-degrading enzyme, which is required for ef
60 of 3 mm glucose, exogenously added bovine or human insulin do not stimulate endogenous insulin secret
62 adapted an existing commercial kit (Mercodia Human Insulin ELISA, 10-1113-01) to quantify insulin fro
64 ten lack characteristic sequence features of human insulin essential for its folding, structure, and
65 t study, we investigated the contribution to human insulin expression of the GG2 motif found between
67 by the atypical responses of T cells to the human insulin fragment that are described by Kent et al.
69 oligonucleotide was demonstrated to capture human insulin from standard solutions and from nuclear e
70 lets by measuring changes in glucose-induced human insulin gene (INS) expression using a single islet
71 em repeats (VNTR) is located upstream of the human insulin gene and correlates with the incidence of
72 uence in the promoter region upstream of the human insulin gene and is widely recognized as a locus o
73 chanism of transcriptional regulation of the human insulin gene by cyclic AMP response element modula
74 engineered to contain multiple copies of the human insulin gene exhibit a large increase in insulin c
75 that AIRE mutation could specifically affect human insulin gene expression in thymic epithelial cells
76 We report 10 heterozygous mutations in the human insulin gene in 16 probands with neonatal diabetes
79 nstrate a critical role for the Z element in human insulin gene transcription and its regulation by g
80 was to characterize the effects of FK506 on human insulin gene transcription, insulin mRNA levels, a
81 more reliable reflection of acute changes to human insulin gene transcriptional rates and that glucos
82 ontrolled by the 5' regulatory region of the human insulin gene was decreased in late passage betaTC-
84 an influence transcriptional activity of the human insulin gene, and thus, may contribute to that por
85 llite, located in the promoter region of the human insulin gene, comprises a variable number of tande
93 cutaneously, [N(epsilon)-palmitoyl Lys(B29)] human insulin had a longer duration of action; a flatter
95 ated insulin [Lys(B29)-lithocholyl des-(B30) human insulin] has been crystallized and the structure d
97 minal prolyl and lysyl residues of wild-type human insulin have been inverted, can be crystallized in
102 d insulin analogues were similar to premixed human insulin in decreasing fasting glucose levels, hemo
107 ct injection of PIP peptides 640 or 250 with human insulin into the lumen of rat jejunum caused a dec
111 engineered monomer ([AspB10, LysB28, ProB29]-human insulin) is determined at neutral pH as a template
115 nged in the absence and presence of elevated human insulin levels (12.6 plus minus 1.2 vs. 12.4 plus
116 M/islets exhibited euglycemia and detectable human insulin levels (157 muU/mL), whereas no human insu
117 304 concentrations also rose with increasing human insulin levels but did not achieve significance in
122 ice were generated in which the cDNA for the human insulin-like growth factor 1B (IGF-1B) was placed
124 ture of a metastable folding intermediate of human insulin-like growth factor I (IGF-I) and an engine
127 es in the cytoplasmic domain of an oncogenic human insulin-like growth factor I receptor (gag-IGFR) w
128 en developed which binds specifically to the human insulin-like growth factor I receptor (IGF-IR) and
129 domains of the Drosophila insulin receptor, human insulin-like growth factor I receptor, and human i
130 dequate delivery of administered recombinant human insulin-like growth factor I to other tissues, inc
136 tudy, we used transgenic mice overexpressing human insulin-like growth factor-1 exclusively in skelet
138 d accumulation (up to 5.8 fold; P < 0.05) of human insulin-like growth factor-binding protein-3 in mo
139 mac25 propeptide shares a 20-25% identity to human insulin-like growth factor-binding proteins (IGFBP
141 ne encoding a dominant-negative, kinase-dead human insulin-like growth factor-I receptor (IGF-IR) tha
142 ccur following administration of recombinant human insulin-like growth factor-I to the intact animal.
144 In contrast to exogenously administered human insulin, LY demonstrated preferential hepatic effe
145 ibe an alternative open reading frame within human insulin mRNA encoding a highly immunogenic polypep
146 les consistently showed the highest level of human insulin mRNA expression and luciferase protein exp
147 kinetics of fibril formation of 20 different human insulin mutants at both low pH (conditions favorin
148 Dogs received 0.36 units/kg s.c. regular human insulin (n = 6) or 1 mg (2.8 units/kg) or 2 mg (5.
150 e that hyperglycaemia impairs the actions of human insulin on umbilical vein endothelial cells isolat
152 and 38 from other sources) if they involved human insulins or insulin analogues, were at least 4 wee
153 ulin analog Lys(B29)-tetradecanoyl des-(B30) human insulin, or NN304, as a marker for insulin transpo
154 sulin were readily differentiated, including human insulin (P28K29) and Lispro insulin (K28P29), whic
157 ovision of an unlimited source of functional human insulin-producing cells and 2) prevention of rejec
158 ls, thereby providing an unlimited source of human insulin-producing cells for basic biochemical stud
160 mice express SOCS-1 under the control of the human insulin promoter and are on the C57BL6/J backgroun
161 ingly, while Pdx1 responsive elements in the human insulin promoter conform to the pentanucleotide 5'
162 ere observed in transgenic mice containing a human insulin promoter fragment, pointing to the respons
163 does not explain all of the activity of the human insulin promoter in cultured islets, and other tra
166 ment between base pairs -341 and -260 of the human insulin promoter, the same region in which a trans
167 n and substitution mutations of the proximal human insulin promoter, we mapped a metabolic response e
168 FK506 decreased HIT cell expression of the human insulin promoter-CAT reporter gene by 40% in the p
169 nt, insulin mRNA levels, and expression of a human insulin promoter-chloramphenicol acetyl transferas
173 cted with an expression plasmid encoding the human insulin receptor (CHO/HIRc) at concentrations wher
175 levels of native and misfolded forms of the human insulin receptor (hIR) and a human variant found i
176 vectors that the 5'-UTR of the mRNA encoding human insulin receptor (hIR) contains a functional IRES.
177 The cytoplasmic juxtamembrane domain of the human insulin receptor (hIR) contains a single copy of t
182 rat fibroblast cell line overexpressing the human insulin receptor (HIRc-B), SHIP inhibited membrane
183 Rat1 fibroblasts transfected with wild-type human insulin receptor (HIRcB) and a truncated receptor
184 ial cell (EC)-specific overexpression of the human insulin receptor (hIRECO) using the Tie2 promoter-
185 TMD and intracellular domain of the soluble human insulin receptor (HIRs) with constant domains from
186 eated rat hepatic tumor cell line expressing human insulin receptor (HTC-IR) and livers from lean and
187 covalently to the cytoplasmic domain of the human insulin receptor (IR) beta-subunit when cells are
189 81, compound 1), which induced activation of human insulin receptor (IR) tyrosine kinase and mediated
190 f Chinese hamster ovary cells expressing the human insulin receptor and differentiated 3T3L1 adipocyt
191 imulated tyrosine autophosphorylation of the human insulin receptor and hDIR, and both receptors medi
192 ptor binding to CHO-T cells transfected with human insulin receptor and in vivo metabolic clearance r
193 n Chinese hamster ovary cells expressing the human insulin receptor and murine 3T3L1 adipocytes, insu
196 he function of a chimeric DIR containing the human insulin receptor binding domain (hDIR) was investi
198 tations in the tyrosine kinase domain of the human insulin receptor frequently result in a dominantly
199 a subunits in the (alpha beta)2 dimer of the human insulin receptor have been identified by labeling
200 he affinity of N-lithocholyl insulin for the human insulin receptor is not significantly diminished.
201 In contrast, transfection of malfunctioning human insulin receptor mutants, identified originally fr
202 f Chinese hamster ovary cells expressing the human insulin receptor resulted in a time-dependent decr
203 A resolution of an amino-terminal segment of human insulin receptor substrate 1 that encompasses its
206 The most commonly detected polymorphism in human insulin receptor substrate-1 (IRS-1), a glycine to
209 screen for small molecules that activate the human insulin receptor tyrosine kinase, a nonpeptidyl fu
210 ucture of the purified, functionally active, human insulin receptor using negative stain and cryo-ele
211 r, we incubated CHO cells overexpressing the human insulin receptor with an antibody to the extracell
212 n Chinese hamster ovary cells expressing the human insulin receptor, both proteins display a diffuse,
213 sis was evaluated directly using recombinant human insulin receptor, hamster beta 2-adrenergic recept
214 n Chinese hamster ovary cells expressing the human insulin receptor, insulin causes decreased phospho
215 hamster ovary cells expressing the wild-type human insulin receptor, mock-transfected cells, cells ex
217 g the cytoplasmic kinase domain (CKD) of the human insulin receptor, we demonstrate that autophosphor
218 f the 83-14 monoclonal antibody (mAb) to the human insulin receptor, which is tagged with streptavidi
227 ovary (CHO) cells that overexpress wild-type human insulin receptors (CHO-hIR-WT) or mutant insulin r
232 inese hamster ovary (CHO-T) cells expressing human insulin receptors and COS-1 cells in response to i
233 inese hamster ovary cells (CHO-T) expressing human insulin receptors causes an 8-10-fold increase in
234 Rat-1 fibroblasts that overexpresses normal human insulin receptors, binding of the GTP analogue GTP
236 reover, the CTL primed with either bovine or human insulin recognize an A-chain peptide that is ident
238 d the contribution of variation in SORCS1 to human insulin-related traits in two distinct Mexican-Ame
240 amide, or PD128763 increased expression of a human insulin reporter gene suppressed by elevated gluco
241 ation in two complementary in vivo models of human insulin resistance (endothelial specific and whole
242 ously hypertensive (SHRSP) rat is a model of human insulin resistance and is characterized by reduced
243 abolic and signaling changes associated with human insulin resistance and provides a genetically amen
246 icate resistin in the pathophysiology of the human insulin resistance syndrome, an effect mediated by
253 unogenicity of insulin lispro versus regular human insulin (RHI) in patients previously treated with
256 excess glucose or lipid influence mouse and human insulin secretion and beta cell activity and show
259 ific CD4(+)T cells and demonstrate efficient human insulin-specific Foxp3(+)Treg-induction upon subim
261 response to [N(epsilon)-palmitoyl Lys(B29)] human insulin support the development and further testin
263 tal composition comprising 75% C8-HI and 25% human insulin that exhibits near-ideal basal pharmacodyn
264 s less with insulin lispro than with regular human insulin therapy during three of four quarters of t
266 ting analog, [N(epsilon)-palmitoyl Lys(B29)] human insulin, to serum albumin in vitro, and the time a
267 addition of 100 nm bovine insulin or 500 nm human insulin together with 3 mm glucose had no stimulat
268 Overexpression of ins-1, or expression of human insulin under the control of ins-1 regulatory sequ
269 e used to extend the time action of insulin, human insulin was acylated at the epsilon-amino group of
271 uman insulin levels (157 muU/mL), whereas no human insulin was detected in the islet-only transplanta
273 In group 2 (n = 6), starting at time 0, human insulin was infused at a pharmacologic dose (60 pm
274 ted immediately before the meal, and regular human insulin was injected 30-45 min before the meal.
278 n for the anti-relaxin antibody, whereas the human insulin was transformed into a bona fide relaxin.
279 nous glucose production (EGP) in nondiabetic humans, insulin was infused at rates of 0.25, 0.375, or
280 proteolytic processing to CpepGFP and native human insulin, which are specifically detected and cosec
282 ne Hagedorn) crystalline complex formed with human insulin, which is commonly used as the long-acting
284 ether the isolated A and B chain peptides of human insulin would form fibrils at neutral and acidic p
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