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1 do not function as allosteric activators of glucokinase.
2 -like domain was identified to interact with glucokinase.
3 xidation/utilization, and phosphorylation by glucokinase.
4 because of inadequate activation of hepatic glucokinase.
5 e the non-Michaelis-Menten behavior of human glucokinase.
6 id not largely differ from that of wild-type glucokinase.
7 e to the apparent absence of a gene encoding glucokinase.
8 hat is 12-fold higher than that of wild-type glucokinase.
9 -PTS activity and expression of the gene for glucokinase.
10 ed for silencing of the key metabolic enzyme glucokinase.
11 -against-all in silico mutagenesis for human glucokinase.
12 (cat)/K(m) value displayed by native E. coli glucokinase.
13 f glucose on the subcellular distribution of glucokinase.
14 s the insulin-sensitive FOXO1 corepressor of glucokinase.
15 he k(cat)/K(m) value of endogenous bacterial glucokinase.
16 ession of Hex-C, a homolog of the MODY2 gene Glucokinase.
17 and the physiological glucose-sensing enzyme glucokinase.
18 low affinity glucose-phosphorylating enzyme glucokinase.
19 stigate the conformational dynamics of human glucokinase, a 52 kDa monomeric enzyme that displays kin
20 have previously been reported to have potent glucokinase-activating properties that exceed the in vit
21 he increase in glucose uptake resulting from glucokinase activation in hepatocytes in vitro translate
28 have investigated the acute actions of novel glucokinase activator compound 50 (GKA50) on islet funct
29 f stability, activity index, the response to glucokinase activator drug, and the effect of glucokinas
30 glucokinase activity was increased, using a glucokinase activator drug, or decreased, using RNA inte
32 Finally, administration of a small molecule glucokinase activator to old mice doubled the frequency
33 lead to the identification of 19 as a potent glucokinase activator with a greater than 50-fold liver-
34 ycogen synthesis with glucose and insulin or glucokinase activator, which resulted in channeling gluc
41 ee principal parts of the new small molecule glucokinase activators led to a robust SAR in agreement
42 y by applying our methodology to a series of glucokinase activators that could be useful for treating
43 es on a carboxylic acid containing series of glucokinase activators with preferential activity in hep
44 that enhance SGU in diabetic patients (e.g. glucokinase activators) are likely to improve glucose to
49 , resulting in diminished mitochondria-based glucokinase activity and blunted mitochondrial respirati
50 domain, significantly reduced both intrinsic glucokinase activity and glucose-induced insulin secreti
51 ents and may allow yeast to rapidly modulate glucokinase activity as nutrient availability changes.
57 by hormones and metabolites of glucose, and glucokinase activity is dependent on reversible binding
60 critical regulator of neuronal glucosensing, glucokinase activity was increased, using a glucokinase
68 ic phosphofructokinases (ADP-PFKs), specific glucokinases (ADP-GKs), and bifunctional enzymes (ADP-PF
71 asmic reticulum (ER)-localized ADP-dependent glucokinase (ADPGK) has been shown to play a critical ro
72 ted in granule fusion, also colocalized with glucokinase after hypotonic lysis or detergent extaction
73 nous insulin or gene transfer for insulin or glucokinase alone failed to achieve complete correction
75 a(+)-dependent secondary active transport, a glucokinase and enzymes of the pentose phosphate pathway
76 iched for the glucose phosphorylating enzyme glucokinase and for genes encoding other enzymes involve
77 uctase), while genes involved in glycolysis (glucokinase and glycerol kinase) were decreased in L-Fab
78 ted viral vectors of serotype 1 encoding for glucokinase and insulin in diabetic dogs resulted in nor
79 " in skeletal muscle through coexpression of glucokinase and insulin, increasing glucose uptake and c
83 r analyses confirmed the interaction between glucokinase and the ubiquitin-like domain in insulin-sec
84 ht into the evolutionary relationship of ROK glucokinases and non-ROK glucokinases (Pfam 02685), reve
85 due in part to reduced expression of hepatic glucokinase, and hyperammonemia from reduced expression
86 n of pancreatic duodenal hemeobox-1 (PDX-1), glucokinase, and insulin-1 was increased as a result of
87 retion pathway including PC1/3, PC2, GLUT-1, glucokinase, and K-ATP channel complex (Sur1 and Kir6.2)
88 activated receptor gamma coactivator 1 beta, glucokinase, and microsomal triacylglycerol transfer pro
90 ucose-sensing neurons (13.5%), which express glucokinase, and the selective urocortin 3 (UCN3) recept
91 erefore, it appears that K(ATP) channels and glucokinase are expressed in GnRH neurons, which renders
93 y implicated in mitochondrial recruitment of glucokinase, as a significant factor influencing the lev
94 s show glucose-responsive insulin secretion, glucokinase association with the granules and low-densit
95 e-2/fructose-2,6-bisphosphatase)/FDPase-2, a glucokinase-binding protein, and glyceraldehyde phosphat
97 s enzyme, and a major unanswered question in glucokinase biology is how post-translational modificati
99 ases in the expression of the glucose sensor glucokinase, but decreases in that of two transcription
101 sucrose gradient centrifugation showed that glucokinase colocalized with the granule membrane marker
102 results provide the first direct evidence of glucokinase conformational heterogeneity and hence shed
103 optotic BCL-2 family member BAD resides in a glucokinase-containing complex that regulates glucose-dr
105 est that structural rearrangements linked to glucokinase cooperativity involve a substrate-induced re
106 f these mechanisms is sufficient to describe glucokinase cooperativity, a transient-state kinetic ana
107 neurons in the ventromedial hypothalamus in glucokinase-Cre mice, which express Cre in glucose-sensi
109 bined with in vivo functional selection in a glucokinase-deficient bacterium to identify four indepen
110 ited to provide new functions, we placed the glucokinase-deficient bacterium under selection for grow
111 f the alsK gene relieves the auxotrophy of a glucokinase-deficient bacterium, demonstrating that weak
112 he loop, coupled with genetic selection in a glucokinase-deficient bacterium, uncovers a hyperactive
113 sensing is conventionally thought to involve glucokinase-dependent metabolism of glucose to ATP, whic
114 glucose-6-phosphatase and the repression of glucokinase during fasting, thus increasing lipogenesis
115 rmacologic targeting of potential downstream glucokinase effectors revealed that ATP-sensitive potass
117 lar signaling of adult tissues and regulates glucokinase enzyme activity in pancreatic beta cells.
118 re glucokinase positive, and the identity of glucokinase-expressing cells remains to be determined.
119 -sensing region that contains characteristic glucokinase-expressing glucose-sensing neurons that resp
120 IRS-1 was also associated with a decrease in glucokinase expression and a trend toward increased bloo
122 hepatic glucose recycling via suppression of glucokinase expression in the basal state to preserve he
124 , reduced expression of PEPCK, and increased glucokinase expression resulting in reduced hepatic gluc
125 d gluconeogenic enzymes is impaired, hepatic glucokinase expression, incorporation of 14C-glucose int
127 glucose metabolism revealed that the hepatic glucokinase flux was decreased by 95% in L-G6pc(-/-) mic
128 found that Glk1, a Saccharomyces cerevisiae glucokinase, forms two-stranded filaments with ultrastru
131 s of hepatic glucose fluxes revealed reduced glucokinase (GCK) and glycogen synthase fluxes as compar
132 nantly nuclear protein that inhibits hepatic glucokinase (GCK) and plays a critical role in glucose h
139 Patients with heterozygous, inactivating glucokinase (GCK) mutations have mild fasting hyperglyce
140 as been useful for identifying patients with glucokinase (GCK) mutations which cause lifelong persist
143 messenger RNA (mRNA) expression of KLF6 and glucokinase (GCK), as an important mediator of insulin s
144 (egr-1), involved in mitogenic response, and glucokinase (Gck), encoding a key metabolic enzyme.
146 (K140E) and Gck(P417R)) in the gene encoding glucokinase (Gck), the mammalian glucose sensor that is
148 d intravenous glucose loads in patients with glucokinase (GCK)-diabetes (MODY2) and hepatocyte nuclea
149 ditional subjects with HNF1A-MODY (n = 188), glucokinase (GCK)-MODY (n = 118), hepatocyte nuclear fac
155 glucose, in line with decreases in Glut2 and glucokinase gene expression, and attenuated glucose-stim
156 ng that icv FGF1 treatment increases hepatic glucokinase gene expression, we considered the possibili
157 A previously proposed hypothesis that the glucokinase gene might be expressed in the pituitary cor
158 stimulated insulin secretion, illustrated by glucokinase gene mutations causing monogenic diabetes an
159 ehensive analysis of common variation of the glucokinase gene shows that this is the first gene to be
160 e transcription but blunted the induction of glucokinase gene transcription and completely blocked th
161 tagenesis screen identified glcK, a putative glucokinase gene, required for beta-d-allose-mediated in
162 to T transversion mutation in exon 9 of the glucokinase gene, resulting in an isoleucine to phenylal
166 ring VMH glucosensing by raising or lowering glucokinase (GK) activity failed to affect spontaneous f
168 ucose, hepatic glycogen content, and hepatic glucokinase (GK) activity/expression as well as higher e
169 gered an increase in the activity of hepatic glucokinase (GK) and glycogen synthase (GS), which occur
172 ized glucosensing neurons, many of which use glucokinase (GK) as the rate-limiting step in glucose's
174 other virus expressing an siRNA specific for glucokinase (GK) caused 80% suppression of GK mRNA and 5
176 ty (ZDF) rats whether restoration of hepatic glucokinase (GK) expression would alter hepatic glucose
183 orted a novel approach to increase cytosolic glucokinase (GK) levels through the binding of a small m
184 trient sensing between beta-cells, including glucokinase (GK) levels, mitochondrial function, or expr
186 The transient kinetics of glucose binding to glucokinase (GK) was studied using stopped-flow fluoresc
189 ivity with glucose is a key feature of human glucokinase (GK), allowing its crucial role as a glucose
190 actate, and express both the glucose sensor, glucokinase (GK), and the SUR1 subunit of the plasma mem
195 mide (51) that was a potent disruptor of the glucokinase-glucokinase regulatory protein (GK-GKRP) int
200 an important CNS glucose sensor, we studied glucokinase-heterozygous knockout mice, but found that t
201 , adenosine deaminase complexing protein 2); glucokinase (hexokinase 4) regulator; guanylate cyclase
203 iveness to diazoxide varies with genotype in glucokinase hyperinsulinism resulting in hypoglycemia, w
208 ver, pharmacologic and genetic activation of glucokinase in the arcuate nucleus of rodent models incr
210 the catalytic activity of recombinant human glucokinase in vitro and also of glucokinase in target c
212 orexin cell glucose sensing is unaffected by glucokinase inhibitors alloxan, d-glucosamine, and N-ace
214 olarization and inhibition are unaffected by glucokinase inhibitors such as alloxan, D-glucosamine, a
215 stent with their documented insensitivity to glucokinase inhibitors, the glucose responses of orexin
218 nd hPXR mice exhibited impaired induction of glucokinase involved in glucose utilization and displaye
225 nt of GKRP with altered binding affinity for glucokinase is associated with increased blood and liver
229 we show that the pancreatic isoform of human glucokinase is SUMOylated in vitro, using recombinant en
230 ucose is metabolized in alpha-cells and that glucokinase is the likely rate-limiting step in this pro
232 mechanistically, as the FOXO1 corepressor of glucokinase is unknown, and clinically, as inhibition of
234 rol subjects (euinsulinemia and euglycemia), glucokinase-maturity-onset diabetes of the young (GCK-MO
239 ary VMH neuronal cultures, the expression of glucokinase mRNA and the number of demonstrable glucosen
240 e RNA did not affect survival but did reduce glucokinase mRNA by 90% in association with loss of all
242 o, a subpopulation of GnRH neurons expressed glucokinase mRNA, a marker for glucose sensitivity.
243 re observed in mice expressing an activating glucokinase mutation, in in vitro models of hyperglycaem
244 relationship of ROK glucokinases and non-ROK glucokinases (Pfam 02685), revealing the primary sequenc
245 substitutions colocalize to a region of the glucokinase polypeptide where a synthetic allosteric act
246 No evidence was found that corticotrophs are glucokinase positive, and the identity of glucokinase-ex
248 cterized by high activities of fructokinase, glucokinase, pyruvate kinase, and tricarboxylic acid cyc
249 ation optimized spectra of uniformly labeled glucokinase, recorded in the absence and presence of glu
251 transmembrane 6 superfamily member 2), GCKR (glucokinase regulator), and HCC in patients treated with
252 bound O-acyltransferase domain containing 7, glucokinase regulator, and hydroxysteroid 17-beta dehydr
254 riation in the apolipoprotein A5 (APOA5) and glucokinase regulatory protein (GCKR) genes has been ass
256 nfirmed association of a SNP in an intron of glucokinase regulatory protein (GCKR) with serum triglyc
257 (NCAN), lysophospholipase-like 1 (LYPLAL1), glucokinase regulatory protein (GCKR), and protein phosp
258 rphism (SNP) identified as rs1260326, in the glucokinase regulatory protein (GCKR), was associated wi
259 ese activators relieved GK's inhibition from glucokinase regulatory protein (GKRP) in a glucose-depen
260 nity and/or by alleviating the inhibition of glucokinase regulatory protein (GKRP), a key regulator o
262 glucokinase to a specific inhibitor protein, glucokinase regulatory protein (GKRP), and to other bind
265 the liver where its activity is regulated by glucokinase regulatory protein (GKRP; gene name GCKR).
266 1.12-1.21; P = 2.24 x 10(-10)), rs1260326 in glucokinase regulatory protein (OR, 1.12; 95% CI, 1.07-1
268 , prevented inhibition of enzyme activity by glucokinase regulatory protein and corresponded with red
270 st the stabilizing protein interactions with glucokinase regulatory protein, which may contribute to
271 LD hepatocytes and inversely correlates with glucokinase regulatory protein, which negatively regulat
275 ermeabilization with digitonin, 50% of total glucokinase remained bound intracellularly, while 30% wa
276 insulin secretion, glucose or inhibitors of glucokinase, respectively, were infused into the third v
278 rocarbon-stapled BAD BH3 helices that target glucokinase, restore glucose-driven mitochondrial respir
279 ansfection of neurons with small interfering glucokinase RNA did not affect survival but did reduce g
281 kinetic model presented herein suggests that glucokinase samples multiple conformations in the absenc
282 x alpha13 and the functional dynamics of the glucokinase scaffold that are required for allostery.
283 They also identify novel features of the glucokinase scaffold that could be targeted during the d
286 compete strongly with glucose for binding to glucokinase, the key glycolysis enzyme presumably active
288 tivity is dependent on reversible binding of glucokinase to a specific inhibitor protein, glucokinase
290 Unexpectedly, the K(m glucose) value of a glucokinase variant lacking alpha13 is equivalent to the
291 n Pten(+/-) mice, hepatic gene expression of glucokinase was 10-fold less than wild-type (Pten(+/+))
293 ctionation of the organelles, immunoreactive glucokinase was distributed approximately equally betwee
294 mulate hepatic glucose uptake; activation of glucokinase was restored and insulin action was improved
295 on of the insulin-responsive GLUT 4, but not glucokinase, was reduced by 30% in NIRKO mice while regi
299 F, and YcfX proteins function as rudimentary glucokinases with ambiguous substrate specificites, disp
300 on of SIN3A abolishes nutrient regulation of glucokinase without affecting other FOXO1 target genes a