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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 ession of Hex-C, a homolog of the MODY2 gene Glucokinase.
8 e to the apparent absence of a gene encoding glucokinase.
9 hat is 12-fold higher than that of wild-type glucokinase.
10 and the physiological glucose-sensing enzyme glucokinase.
11 ed for silencing of the key metabolic enzyme glucokinase.
12 -against-all in silico mutagenesis for human glucokinase.
13 (cat)/K(m) value displayed by native E. coli glucokinase.
14 f glucose on the subcellular distribution of glucokinase.
15 he k(cat)/K(m) value of endogenous bacterial glucokinase.
16  in the theoretical model of human beta-cell glucokinase.
17  low affinity glucose-phosphorylating enzyme glucokinase.
18 s the insulin-sensitive FOXO1 corepressor of 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
22                              Arcuate nucleus glucokinase activation may represent a CNS mechanism tha
23 ave been synthesized and tested in vitro for glucokinase activation potential.
24                                 In contrast, glucokinase activation stimulated Cn-dependent expressio
25                                Compound 1, a glucokinase activator (GKA) lead that we have previously
26           A short and practical synthesis of glucokinase activator 1 was achieved utilizing a converg
27                                            A glucokinase activator acutely restored cytochrome c redu
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
31                            A pharmacological glucokinase activator produced a dose-related increase i
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
35         PKCzeta is required for glucose- and glucokinase activator-induced proliferation of rodent an
36 g anti-hyperglycemic agents that function as glucokinase activators (GKAs).
37 nd initial optimization of a novel series of glucokinase activators (GKAs).
38 optimization of a novel series of allosteric glucokinase activators (GKAs).
39                          Systemically acting glucokinase activators (liver and pancreas) have been re
40                            Insulin-releasing glucokinase activators and pancreatic-G-protein-coupled
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
45  novel bidentate anchor point for allosteric glucokinase activators.
46 atory evolution was conducted to improve the glucokinase activities of AlsK and NanK.
47 lypeptides, all of which possess rudimentary glucokinase activities.
48                        Additionally, altered glucokinase activity affected release of the orexigenic
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                                   Subsequent glucokinase activity assays of the glcK mutant further s
52            This increase provides sufficient glucokinase activity for reconstitution of the defunct g
53           Together, our results suggest that glucokinase activity in the arcuate nucleus specifically
54  by hormones and metabolites of glucose, and glucokinase activity is dependent on reversible binding
55  in the alsK and nanK genes that improve the glucokinase activity of each enzyme.
56 e ingestion, while decreased arcuate nucleus glucokinase activity reduced glucose intake.
57 critical regulator of neuronal glucosensing, glucokinase activity was increased, using a glucokinase
58                              In fasted rats, glucokinase activity was specifically increased in the a
59 hibited (IC(50) of 2.0 micro mol/l), whereas glucokinase activity was unaffected at drug levels as hi
60                     Here, we determined that glucokinase activity within the hypothalamic arcuate nuc
61     Liver glucose metabolism is dependent on glucokinase activity.
62 phosphorylation status of BAD helps regulate glucokinase activity.
63 on in MIN6 cells but had only some effect on glucokinase activity.
64                                              Glucokinase acts as a glucose sensor in pancreatic beta
65                                ADP-dependent glucokinase (ADPGK) catalyzes glucose-6-phosphate produc
66 ted in granule fusion, also colocalized with glucokinase after hypotonic lysis or detergent extaction
67 nous insulin or gene transfer for insulin or glucokinase alone failed to achieve complete correction
68                       To examine the role of glucokinase, an important CNS glucose sensor, we studied
69 a(+)-dependent secondary active transport, a glucokinase and enzymes of the pentose phosphate pathway
70 uctase), while genes involved in glycolysis (glucokinase and glycerol kinase) were decreased in L-Fab
71 ted viral vectors of serotype 1 encoding for glucokinase and insulin in diabetic dogs resulted in nor
72 " in skeletal muscle through coexpression of glucokinase and insulin, increasing glucose uptake and c
73 he shunt pathway, and lipogenesis, including glucokinase and SREBP-1c.
74 sulin-processing enzymes, beta-cell-specific glucokinase and sulfonylurea receptor.
75 r analyses confirmed the interaction between glucokinase and the ubiquitin-like domain in insulin-sec
76 ht into the evolutionary relationship of ROK glucokinases and non-ROK glucokinases (Pfam 02685), reve
77 cose-6-phosphatase and suppression of GLUT2, glucokinase, and glycerol-3-phosphate dehydrogenase.
78 due in part to reduced expression of hepatic glucokinase, and hyperammonemia from reduced expression
79 n of pancreatic duodenal hemeobox-1 (PDX-1), glucokinase, and insulin-1 was increased as a result of
80 retion pathway including PC1/3, PC2, GLUT-1, glucokinase, and K-ATP channel complex (Sur1 and Kir6.2)
81 activated receptor gamma coactivator 1 beta, glucokinase, and microsomal triacylglycerol transfer pro
82 e also found to bind to amyloid polypeptide, glucokinase, and pax-4 control sequences in vivo.
83 ylase, fatty acid synthase, SREBP1c, chREBP, glucokinase, and pyruvate kinase.
84 ucose-sensing neurons (13.5%), which express glucokinase, and the selective urocortin 3 (UCN3) recept
85 erefore, it appears that K(ATP) channels and glucokinase are expressed in GnRH neurons, which renders
86         These results confirm the potency of glucokinase as the pancreatic beta-cell glucose sensor,
87 y implicated in mitochondrial recruitment of glucokinase, as a significant factor influencing the lev
88 s show glucose-responsive insulin secretion, glucokinase association with the granules and low-densit
89 e-2/fructose-2,6-bisphosphatase)/FDPase-2, a glucokinase-binding protein, and glyceraldehyde phosphat
90 hybrid library was produced and searched for glucokinase-binding proteins.
91 s enzyme, and a major unanswered question in glucokinase biology is how post-translational modificati
92 1-4 (Glut1-4), phosphoglycerate kinase 1 and Glucokinase but not of prolyl hydroxylase isoforms.
93 ases in the expression of the glucose sensor glucokinase, but decreases in that of two transcription
94 pc2 opposes the action of the glucose sensor glucokinase by hydrolyzing G6P.
95  sucrose gradient centrifugation showed that glucokinase colocalized with the granule membrane marker
96 results provide the first direct evidence of glucokinase conformational heterogeneity and hence shed
97 optotic BCL-2 family member BAD resides in a glucokinase-containing complex that regulates glucose-dr
98                                Polyphosphate glucokinase converts glucose to glucose-6-phosphate usin
99 est that structural rearrangements linked to glucokinase cooperativity involve a substrate-induced re
100 f these mechanisms is sufficient to describe glucokinase cooperativity, a transient-state kinetic ana
101  neurons in the ventromedial hypothalamus in glucokinase-Cre mice, which express Cre in glucose-sensi
102           Genetic selection experiments in a glucokinase-deficient bacterium identified a variety of
103 bined with in vivo functional selection in a glucokinase-deficient bacterium to identify four indepen
104 ited to provide new functions, we placed the glucokinase-deficient bacterium under selection for grow
105 f the alsK gene relieves the auxotrophy of a glucokinase-deficient bacterium, demonstrating that weak
106 he loop, coupled with genetic selection in a glucokinase-deficient bacterium, uncovers a hyperactive
107 sensing is conventionally thought to involve glucokinase-dependent metabolism of glucose to ATP, whic
108  glucose-6-phosphatase and the repression of glucokinase during fasting, thus increasing lipogenesis
109 rmacologic targeting of potential downstream glucokinase effectors revealed that ATP-sensitive potass
110 -d-mannosamine are largely unaffected by the glucokinase-enhancing substitutions.
111 lar signaling of adult tissues and regulates glucokinase enzyme activity in pancreatic beta cells.
112 re glucokinase positive, and the identity of glucokinase-expressing cells remains to be determined.
113 -sensing region that contains characteristic glucokinase-expressing glucose-sensing neurons that resp
114 IRS-1 was also associated with a decrease in glucokinase expression and a trend toward increased bloo
115                        In humans, changes in glucokinase expression and activity are associated with
116 hepatic glucose recycling via suppression of glucokinase expression in the basal state to preserve he
117 on occurred despite very low levels of liver glucokinase expression in the insulin-deficient STZ-inje
118                                              Glucokinase expression is transcriptionally regulated by
119 eltaC in the background of depressed hepatic glucokinase expression suggests that controlled stimulat
120 d gluconeogenic enzymes is impaired, hepatic glucokinase expression, incorporation of 14C-glucose int
121 oncomitant upregulation of islet insulin and glucokinase expression.
122 glucose metabolism revealed that the hepatic glucokinase flux was decreased by 95% in L-G6pc(-/-) mic
123 were expressed as glutathionyl S-transferase-glucokinase fusion proteins.
124                                              Glucokinase (GCK) and glucose-6-phosphatase catalytic su
125 s of hepatic glucose fluxes revealed reduced glucokinase (GCK) and glycogen synthase fluxes as compar
126 nantly nuclear protein that inhibits hepatic glucokinase (GCK) and plays a critical role in glucose h
127                                              Glucokinase (GCK) catalyzes the rate-limiting step of gl
128               Mutations in the gene encoding glucokinase (GCK) cause a mild hereditary form of diabet
129                                 Mutations in glucokinase (GCK) cause a spectrum of glycemic disorders
130                                              Glucokinase (GCK) controls the rate of glucose metabolis
131                                              Glucokinase (Gck) is a critical regulator of glucose-ind
132                                              Glucokinase (GCK) is a key regulatory enzyme in the panc
133     Patients with heterozygous, inactivating glucokinase (GCK) mutations have mild fasting hyperglyce
134 as been useful for identifying patients with glucokinase (GCK) mutations which cause lifelong persist
135                                              Glucokinase (GCK) regulates glucose storage and disposal
136         Mice haploinsufficient for beta cell glucokinase (Gck) were unable to increase their beta cel
137  messenger RNA (mRNA) expression of KLF6 and glucokinase (GCK), as an important mediator of insulin s
138 (egr-1), involved in mitogenic response, and glucokinase (Gck), encoding a key metabolic enzyme.
139                       Cooperativity in human glucokinase (GCK), the body's primary glucose sensor and
140 (K140E) and Gck(P417R)) in the gene encoding glucokinase (Gck), the mammalian glucose sensor that is
141                              The hallmark of glucokinase (GCK), which catalyzes the phosphorylation o
142 d intravenous glucose loads in patients with glucokinase (GCK)-diabetes (MODY2) and hepatocyte nuclea
143 ditional subjects with HNF1A-MODY (n = 188), glucokinase (GCK)-MODY (n = 118), hepatocyte nuclear fac
144 s AKT and Foxo1, and decreased expression of glucokinase (Gck).
145 istent with post-translational activation of glucokinase (GCK).
146 determinant of fasting glucose is the enzyme glucokinase (GCK).
147 thway culminating in induction of the enzyme glucokinase (GCK).
148 zygous loss of function of the gene encoding glucokinase (GCK).
149 glucose, in line with decreases in Glut2 and glucokinase gene expression, and attenuated glucose-stim
150    A previously proposed hypothesis that the glucokinase gene might be expressed in the pituitary cor
151 stimulated insulin secretion, illustrated by glucokinase gene mutations causing monogenic diabetes an
152 ehensive analysis of common variation of the glucokinase gene shows that this is the first gene to be
153 e transcription but blunted the induction of glucokinase gene transcription and completely blocked th
154 tagenesis screen identified glcK, a putative glucokinase gene, required for beta-d-allose-mediated in
155  to T transversion mutation in exon 9 of the glucokinase gene, resulting in an isoleucine to phenylal
156                                              Glucokinase (GK) activation as a potential strategy to t
157                                              Glucokinase (GK) activators are currently under investig
158 ucing glucose transporter type 2 (Glut2) and glucokinase (GK) activities.
159 as increased in beta cell lines by enhancing glucokinase (GK) activity and exposing cells to physiolo
160 ring VMH glucosensing by raising or lowering glucokinase (GK) activity failed to affect spontaneous f
161                                              Glucokinase (GK) activity is essential for the physiolog
162                                              Glucokinase (GK) activity plays a key role in glucose-st
163 ucose, hepatic glycogen content, and hepatic glucokinase (GK) activity/expression as well as higher e
164 gered an increase in the activity of hepatic glucokinase (GK) and glycogen synthase (GS), which occur
165                                              Glucokinase (GK) and its inhibitory protein, GK regulato
166                                              Glucokinase (GK) appears to be the primary regulator of
167 ized glucosensing neurons, many of which use glucokinase (GK) as the rate-limiting step in glucose's
168                   However, overactivation of glucokinase (GK) can cause excessive glucose turnover, l
169 other virus expressing an siRNA specific for glucokinase (GK) caused 80% suppression of GK mRNA and 5
170                         Glucose flux through glucokinase (GK) controls insulin release from the pancr
171 ty (ZDF) rats whether restoration of hepatic glucokinase (GK) expression would alter hepatic glucose
172                             Mutations in the glucokinase (GK) gene cause defects in blood glucose hom
173                                              Glucokinase (GK) gene transcription initiates in the isl
174                                              Glucokinase (GK) has several known polymorphic activatin
175                                              Glucokinase (GK) is a glucose sensor that couples glucos
176                                        Human glucokinase (GK) is a principal regulating sensor of pla
177                                              Glucokinase (GK) is hypothesized to be the critical gluc
178                                              Glucokinase (GK) is the rate-limiting step for insulin r
179 orted a novel approach to increase cytosolic glucokinase (GK) levels through the binding of a small m
180                     To better understand how glucokinase (GK) missense mutations associated with huma
181                                              Glucokinase (GK) plays a key role in whole-body glucose
182                                              Glucokinase (GK) serves as glucose sensor in pancreatic
183 The transient kinetics of glucose binding to glucokinase (GK) was studied using stopped-flow fluoresc
184                 Small molecule activators of glucokinase (GK) were used in kinetic and equilibrium bi
185                                              Glucokinase (GK), a key enzyme that regulates glucose ho
186 ivity with glucose is a key feature of human glucokinase (GK), allowing its crucial role as a glucose
187 actate, and express both the glucose sensor, glucokinase (GK), and the SUR1 subunit of the plasma mem
188                                              Glucokinase (GK), the putative glucosensing gatekeeper,
189 rt to decreased glucose-induced flux through glucokinase (GK).
190                  The continuous assay, using glucokinase (Glk) and glucose-6-phosphate dehydrogenase
191 d expression of the GalP permease (galP) and glucokinase (glk).
192  that GI and GE, but not NR, cells expressed glucokinase (GLK).
193                                          The glucokinase-glucokinase regulatory protein (GK-GKRP) com
194 mide (51) that was a potent disruptor of the glucokinase-glucokinase regulatory protein (GK-GKRP) int
195                A nonracemic synthesis of the glucokinase-glucokinase regulatory protein disruptor AMG
196                                     Purified glucokinase had a monomeric molecular mass of 33.8kDa wh
197         Heterozygous activating mutations of glucokinase have been reported to cause hypoglycemia att
198                 Small molecule activators of glucokinase have shown robust efficacy in both preclinic
199  an important CNS glucose sensor, we studied glucokinase-heterozygous knockout mice, but found that t
200 , adenosine deaminase complexing protein 2); glucokinase (hexokinase 4) regulator; guanylate cyclase
201 WAVE-1 as an A kinase anchoring protein, and glucokinase (hexokinase IV).
202        We report three children with de novo glucokinase hyperinsulinism mutations who displayed a sp
203 iveness to diazoxide varies with genotype in glucokinase hyperinsulinism resulting in hypoglycemia, w
204       In one case, an activating mutation of glucokinase (I211F) was found in pathological islets onl
205 ther, these data support a critical role for glucokinase in neuronal glucosensing.
206 cleus and cytoplasm and co-localization with glucokinase in pancreatic beta cells.
207 inant human glucokinase in vitro and also of glucokinase in target cells.
208 ver, pharmacologic and genetic activation of glucokinase in the arcuate nucleus of rodent models incr
209 n and a higher activity of fructokinase than glucokinase in the embryo are both consistent with the e
210  the catalytic activity of recombinant human glucokinase in vitro and also of glucokinase in target c
211 c2a2 (also known as Glut2) and Gck (encoding glucokinase) in beta-cells, which results in defective g
212                                          The glucokinase inhibitor alloxan increases KATP single-chan
213 ansport and glycolysis, in particular by the glucokinase inhibitor glucosamine, blocked the effect of
214 orexin cell glucose sensing is unaffected by glucokinase inhibitors alloxan, d-glucosamine, and N-ace
215                 In contrast, infusion of the glucokinase inhibitors glucosamine or mannoheptulose wor
216 olarization and inhibition are unaffected by glucokinase inhibitors such as alloxan, D-glucosamine, a
217 stent with their documented insensitivity to glucokinase inhibitors, the glucose responses of orexin
218                     Expression of the mutant glucokinase ins454A, W99L, and M197I enzymes revealed a
219                           The secretin, beta-glucokinase, insulin I, and insulin II genes, four known
220 nd hPXR mice exhibited impaired induction of glucokinase involved in glucose utilization and displaye
221                  To test the hypothesis that glucokinase is a critical regulator of neuronal glucosen
222                                              Glucokinase is a key regulator of glucose homeostasis, a
223                                      Because glucokinase is a metabolic sensor involved in the regula
224                                        Human glucokinase is a monomeric enzyme that displays a sigmoi
225                             Human pancreatic glucokinase is a monomeric enzyme that displays kinetic
226                     The results suggest that glucokinase is an integral component of the granule and
227 nt of GKRP with altered binding affinity for glucokinase is associated with increased blood and liver
228                                              Glucokinase is inhibited in the postabsorptive state by
229 g that the synergistic action of insulin and glucokinase is needed for full therapeutic effect.
230                                              Glucokinase is one of the promising targets for glucose-
231 we show that the pancreatic isoform of human glucokinase is SUMOylated in vitro, using recombinant en
232 ucose is metabolized in alpha-cells and that glucokinase is the likely rate-limiting step in this pro
233                                              Glucokinase is the predominant hexokinase expressed in h
234 mechanistically, as the FOXO1 corepressor of glucokinase is unknown, and clinically, as inhibition of
235               Intracellular Mg(2+) regulates glucokinase, KATP channels, and L-type Ca(2+) channels i
236 /Q calcium channel activity are required for glucokinase-mediated glucose intake.
237                                     Impaired glucokinase-mediated glucose phosphorylation in LRH-1-de
238                         It is also the first glucokinase missense mutation reported in mice and is ho
239                                     However, glucokinase mRNA and protein levels as well as fructose-
240 ary VMH neuronal cultures, the expression of glucokinase mRNA and the number of demonstrable glucosen
241 e RNA did not affect survival but did reduce glucokinase mRNA by 90% in association with loss of all
242      IL-6 also decreased refeeding-dependent glucokinase mRNA induction by approximately 40%.
243 o, a subpopulation of GnRH neurons expressed glucokinase mRNA, a marker for glucose sensitivity.
244 re observed in mice expressing an activating glucokinase mutation, in in vitro models of hyperglycaem
245 relationship of ROK glucokinases and non-ROK glucokinases (Pfam 02685), revealing the primary sequenc
246  substitutions colocalize to a region of the glucokinase polypeptide where a synthetic allosteric act
247 No evidence was found that corticotrophs are glucokinase positive, and the identity of glucokinase-ex
248                     In siACC1-treated cells, glucokinase protein levels were decreased by 25%, which
249 cterized by high activities of fructokinase, glucokinase, pyruvate kinase, and tricarboxylic acid cyc
250 ation optimized spectra of uniformly labeled glucokinase, recorded in the absence and presence of glu
251                                        GCKR (glucokinase regulator; P=9.8x10(-10)) and HIF1AN (factor
252 riation in the apolipoprotein A5 (APOA5) and glucokinase regulatory protein (GCKR) genes has been ass
253                                              Glucokinase regulatory protein (GCKR) inhibitors offer a
254 nfirmed association of a SNP in an intron of glucokinase regulatory protein (GCKR) with serum triglyc
255  (NCAN), lysophospholipase-like 1 (LYPLAL1), glucokinase regulatory protein (GCKR), and protein phosp
256 rphism (SNP) identified as rs1260326, in the glucokinase regulatory protein (GCKR), was associated wi
257 ese activators relieved GK's inhibition from glucokinase regulatory protein (GKRP) in a glucose-depen
258 nity and/or by alleviating the inhibition of glucokinase regulatory protein (GKRP), a key regulator o
259                                 GCKR encodes glucokinase regulatory protein (GKRP), a predominantly n
260 glucokinase to a specific inhibitor protein, glucokinase regulatory protein (GKRP), and to other bind
261 by targeting the endogenous inhibitor of GK, glucokinase regulatory protein (GKRP).
262  small molecule to its endogenous inhibitor, glucokinase regulatory protein (GKRP).
263 the liver where its activity is regulated by glucokinase regulatory protein (GKRP; gene name GCKR).
264 1.12-1.21; P = 2.24 x 10(-10)), rs1260326 in glucokinase regulatory protein (OR, 1.12; 95% CI, 1.07-1
265        Allosteric responses to inhibition by glucokinase regulatory protein and activation by the dru
266 , prevented inhibition of enzyme activity by glucokinase regulatory protein and corresponded with red
267                                          The glucokinase regulatory protein encoded by GCKR plays an
268 st the stabilizing protein interactions with glucokinase regulatory protein, which may contribute to
269 LD hepatocytes and inversely correlates with glucokinase regulatory protein, which negatively regulat
270                            Disruption of the glucokinase regulatory protein-binding site (GCK(K140E))
271 lucokinase activator drug, and the effect of glucokinase regulatory protein.
272 vestigated these issues using GCKR, encoding glucokinase regulatory protein.
273 ermeabilization with digitonin, 50% of total glucokinase remained bound intracellularly, while 30% wa
274  insulin secretion, glucose or inhibitors of glucokinase, respectively, were infused into the third v
275 ndent activation of G6pase and inhibition of glucokinase, respectively.
276 rocarbon-stapled BAD BH3 helices that target glucokinase, restore glucose-driven mitochondrial respir
277 ansfection of neurons with small interfering glucokinase RNA did not affect survival but did reduce g
278 r fetal growth, the -30G-->A polymorphism of glucokinase (rs1799884).
279 kinetic model presented herein suggests that glucokinase samples multiple conformations in the absenc
280 x alpha13 and the functional dynamics of the glucokinase scaffold that are required for allostery.
281     They also identify novel features of the glucokinase scaffold that could be targeted during the d
282                                    ASEdb and glucokinase scores are available at http://www.rostlab.o
283                                              Glucokinase steady-state kinetics is unaffected by the e
284 se (3-MG), which cannot be phosphorylated by glucokinase, stimulate TXNIP expression.
285 compete strongly with glucose for binding to glucokinase, the key glycolysis enzyme presumably active
286                            Ligand binding to glucokinase, thrombin, and its precursor prethrombin-2 a
287 tivity is dependent on reversible binding of glucokinase to a specific inhibitor protein, glucokinase
288                                          The glucokinase V62M and G72R mutations are naturally occurr
289    Unexpectedly, the K(m glucose) value of a glucokinase variant lacking alpha13 is equivalent to the
290 n Pten(+/-) mice, hepatic gene expression of glucokinase was 10-fold less than wild-type (Pten(+/+))
291                        Enzymatic activity of glucokinase was demonstrated, quantitated, and character
292 ctionation of the organelles, immunoreactive glucokinase was distributed approximately equally betwee
293 mulate hepatic glucose uptake; activation of glucokinase was restored and insulin action was improved
294 on of the insulin-responsive GLUT 4, but not glucokinase, was reduced by 30% in NIRKO mice while regi
295 c glucose sensing protein expression (GLUTs, glucokinase) were measured.
296 accompanied by an induction in expression of glucokinase, which promotes hepatic glucose utilization.
297                           The association of glucokinase with insulin secretory granules has been sho
298                                Inhibition of glucokinase with mannoheptulose or 5-thioglucose selecti
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

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