MODY2 (mature onset diabetes of the young, type2) is associated with mutations in the GCK gene that result in impaired glucokinase activity. Although more than 200 inactivating GCK mutations have been reported, only less than 20% of these mutations have been functionally characterized. In this work we describe the biochemical characterization of six missense glucokinase mutations associated to MODY2 from Spanish patients, namely Y61S, V182L, C233R, E265K, A379V and K420E. All these mutations produced enzymes that presented reduced enzymatic activity in various degrees, from a mild affectation (K420E) to a more severe effect (C233R). The severity of the mutation correlated with the importance of the structural changes introduced by the mutations. For example, the C233R affected a critical residue of the active centre of the enzyme and rendered a protein with undetectable enzymatic activity. These data add new information on the structure-function relationship of human glucokinase ...
We describe a novel homozygous missense glucokinase mutation (R397L) resulting in insulin-treated neonatal diabetes in an infant from a consanguineous Asian family. Both parents were heterozygous for R397L and had mild hyperglycemia. Glucokinase mutations should be considered in infants of all ethnic groups with neonatal diabetes and consanguinity.
The glucokinase regulatory protein (GKRP) also known as glucokinase (hexokinase 4) regulator (GCKR) is a protein produced in hepatocytes (liver cells). GKRP binds and moves glucokinase (GK), thereby controlling both activity and intracellular location of this key enzyme of glucose metabolism. GKRP is a 68 kD protein of 626 amino acids. It is coded for by a 19 exon gene, GCKR, on the short arm of chromosome 2 (2p23). GKRP was discovered by Emile van Schaftingen and reported in 1989 Glucokinase (GK) in liver cells phosphorylates glucose, preparing it for incorporation into glycogen. During periods of ample glucose supply, most GK activity can be found in the peripheral cytoplasm where glycogen synthesis is occurring. As the glucose supply declines during periods of fasting, GK activity in the cytoplasm diminishes. GKRP participates in this modulation of GK activity and location by binding free cytoplasmic GK as glucose levels decline, and moving it into the nucleus, where it is held in reserve in ...
Buy our Recombinant Human Glucokinase protein. Ab73514 is a full length protein produced in Escherichia coli and has been validated in SDS-PAGE. Abcam provides…
Glucokinase (also called GCK, hexokinase type IV or D and ATP: D-hexose 6-phosphotransferase; EC 2.7.1.1) is expressed in specific types of tissues: liver, pancreas, small intestine and brain. Glucokinase functions as a glucose sensor, triggering shifts in carbohydrate metabolism or cell function in response to the levels of glucose in blood, such as nutritional and hormonal molecular pathways. Unlike other Hexokinases, Glucokinase has a relatively low affinity for glucose and it is not inhibited by physiological concentrations of glucose 6-phosphate. Mutations in the gene encoding GCK can cause both hyperglycemia and hypoglycemia. Due to the major role of Glucokinase in controlling blood glucose homeostasis, Glucokinase is currently considered as a strong candidate target for the treatment of Hyperglycemia, a condition encountered in Type 2 Diabetic patients. Assay Genies Glucokinase Activity Assay Kit provides a quick and easy method for monitoring GCK activity in wide variety of samples. In ...
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Soluble rat liver glucokinase was expressed at high levels at 22 degrees C in the BL21(DE3)pLysS strain of Escherichia coli. Aspartate-211 of yeast hexokinase has been implicated as a catalytic residue from crystallographic data. The corresponding residue in rat liver glucokinase, aspartate-205, was mutated to alanine and the expressed mutant had 1/500th of the activity of the wild type, with no change in the Km values for glucose or ATP. The results support a role for this residue as a base catalyst in the glucokinase reaction and, most probably, a similar role in the reactions of all members of the hexokinase family. ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
OBJECTIVE: Inactivating mutations in glucokinase (GCK) cause mild fasting hyperglycemia. Identification of a GCK mutation has implications for treatment and prognosis; therefore, it is important to identify these individuals. A significant number of patients have a phenotype suggesting a defect in glucokinase but no abnormality of GCK. We hypothesized that the GCK beta-cell promoter region, which currently is not routinely screened, could contain pathogenic mutations; therefore, we sequenced this region in 60 such probands. RESEARCH DESIGN AND METHODS: The beta-cell GCK promoter was sequenced in patient DNA. The effect of the identified novel mutation on GCK promoter activity was assessed using a luciferase reporter gene expression system. Electrophoretic mobility shift assays (EMSAs) were used to determine the impact of the mutation on Sp1 binding. RESULTS: A novel -71G|C mutation was identified in a nonconserved region of the human promoter sequence in six apparently unrelated probands. Family testing
Mutants of Saccharomyces cerevisiae lacking glucokinase (EC 2.7.1.2) have no discernible phenotypic difference from the wild-type strain; in a hexokinaseless background, however, they are unable to grow on any sugar except galactose. Reversion studies with glucokinase mutants indicate that the yeast S. cerevisiae has no other enzyme for phosphorylating glucose except the two hexokinases, P1 and P2, and glucokinase. Spontaneous revertants of hxk1 hxk2 glk1 strains collected on glucose regain any one of these three enzymes. The majority of glucokinase revertants synthesize species of enzyme activity that are kinetically or otherwise indistinguishable from the wild-type enzyme. In a few cases the reverted enzyme is very perceptibly altered in properties with a Km for glucose two orders of magnitude higher than that of the enzyme from the wild-type parent. These recessive, noncomplementing mutants, thus, define a single structural gene GLK1 of glucokinase. Yeast diploids lacking all of the three ...
Median HbA1c was 6.9% in patients with the GCK mutation, 5.8% in controls, and 7.8% in patients with YT2D. Patients with GCK had a low prevalence of clinically significant microvascular complications (1% [95% CI, 0%-5%]) that was not significantly different from controls (2% [95% CI, 0.3%-8%], P=.52) and lower than in patients with YT2D (36% [95% CI, 25%-47%], P,.001). Thirty percent of patients with GCK had retinopathy (95% CI, 21%-41%) compared with 14% of controls (95% CI, 7%-23%, P=.007) and 63% of patients with YT2D (95% CI, 51%-73%, P,.001). Neither patients with GCK nor controls required laser therapy for retinopathy compared with 28% (95% CI, 18%-39%) of patients with YT2D (P,.001). Neither patients with GCK patients nor controls had proteinuria and microalbuminuria was rare (GCK, 1% [95% CI, 0.2%-6%]; controls, 2% [95% CI, 0.2%-8%]), whereas 10% (95% CI, 4%-19%) of YT2D patients had proteinuria (P,.001 vs GCK) and 21% (95% CI, 13%-32%) had microalbuminuria (P,.001). Neuropathy was rare ...
FIG. 3. Threshold shift of GSIR due to A456V. A comparison of wild-type and mutant enzyme kinetics is shown in A, and the relative β-cell glucose phosphorylation rate (rel. BGPR) is plotted in B as a function of blood glucose. The wild-type/wild-type threshold for GSIR is by definition 5 mmol/l (GSIR-5) and, in this study, is reached at ∼25.7% of the hypothetical maximum of the BGPR. The apparent GSRI-5 for A456V is calculated as 1.5 mmol/l based on adaptation of both GK alleles to low glucose when the rel. BGPR is ∼25.7%. ...
Glucokinase is one of the promising targets for glucose-lowering agents, and the development of GK activators are now considered as one of the most promising strategies for the treatment of type 2 diabetes mellitus. In this work, a series of novel symmetric molecular constructs, in which two pyridoxine moieties are connected via sulfur-containing linkers, have been synthesized and tested in vitro for glucokinase activation potential. The enzyme activation rates by two most active compounds at 100 μM (~150% and 130%) were comparable to that of the reference agent PF-04937319 (~154%). Both leading compounds demonstrated low cytotoxicity and excellent safety profile in acute toxicity experiment in rats after oral administration with LD50 exceeding 2000 mg/kg of body weight. Binding mode of the active compounds in comparison with the reference agent was studied using molecular docking. The leading compounds represent viable preclinical candidates for the treatment of type 2 diabetes mellitus, as ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Fetal malnutrition is associated with development of impaired glucose tolerance, diabetes and hypertension in later life in humans and several mammalian species. The mechanisms that underlie this phenomenon of fetal programming are unknown. We hypothesize that adverse effects in utero and early life may influence the basal expression levels of certain genes such that they are re-set with long-term consequences for the organism. An excellent candidate mechanism for this re-setting process is DNA methylation, since post-natal methylation patterns are largely established in utero. We have sought to test this hypothesis by investigating the glucokinase gene (Gck) in rat offspring programmed using a maternal low protein diet model (MLP). Northern blot reveals that fasting levels of Gck expression are reduced after programming, although this distinction disappears after feeding. Bisulphite sequencing of the hepatic Gck promoter indicates a complete absence of methylation at the 12 CpG sites studied in ...
A new study in the Journal of Clinical Investigation reveals that activation of an enzyme, glucokinase, in a region of the hypothalamus called the arcuate nucleus specifically increases glucose uptake.
Glucokinase is an enzyme that facilitates phosphorylation of glucose to glucose-6-phosphate. Glucokinase occurs in cells in theliver, pancreas, gut, and brain of humans and most other vertebrates. In each of these organs it plays an important role in the regulation of carbohydrate metabolism by acting as a glucose sensor, triggering shifts in metabolism or cell function in response to rising or falling levels of glucose, such as occur after a meal or when fasting. Glucokinase has a lower affinity for glucose than the other hexokinases do, and its activity is localized to a few cell types, leaving the other three hexokinases as more important preparers of glucose for glycolysis and glycogen synthesis for most tissues and organs. Mutations of the gene for this enzyme can cause unusual forms of diabetes or hypoglycemia.. ...
approximately 26 million Americans have diabetes. Current therapies for this progressive disease are insufficient or have unwanted side-effects creating a need for the development of novel therapeutic approaches. About Glucokinase Activation and AMG 151 Glucokinase activators, such as AMG 151, represent a promising new class of drugs for the treatment of Type 2 diabetes. Glucokinase is the enzyme that acts as a glucose sensor in the pancreas and liver. The activation of glucokinase lowers glucose levels by enhancing the ability of the pancreas to sense glucose, which leads to increased insulin production. Simultaneously, GKAs increase the net uptake of blood glucose by the liver. In multiple well-established preclinical models of Type 2 diabetes, AMG 151 was highly efficacious in controlling both fasting and non-fasting blood glucose, with rapid onset of effect and maximal efficacy within five to eight once daily doses. In these studies, when combined with existing standard-of-care drugs ...
Glucokinase is the predominant hexokinase expressed in hepatocytes and pancreatic -cells, with a pivotal part in controlling glucose-stimulated insulin release, illustrated simply by glucokinase gene mutations leading to monogenic congenital and diabetes hyperinsulinemic hypoglycemia. PDX-1 SB-715992 (16), the islet cell autoantigen 512 (17), and the voltage-dependent E+ route Kaviar2.1 (18). Lately, overexpression of SUMO-1 in pancreatic human being and animal -cells was demonstrated to impair glucose-stimulated insulin release (19). In this ongoing work, we record for the 1st period that recombinant GK can be customized by SUMOylation and in insulin-secreting -cell lines (Inches-1 and Minutes6). Both recombinant pancreatic and liver organ hGK had been SUMOylated cells and filtered as referred to previously (20). In Vitro SUMOylation Assay All recombinant aminoacids, except RanBP2FG (Enzo Existence Sciences (Farmingdale, Ny og brugervenlig)), had been from LAE Biotech Essential (Rockville, MD). ...
Epidemiological studies have identified a positive association between prostate cancer and recent onset type 2 diabetes mellitus but an increasingly inverse association with greater duration of type 2 diabetes. The mecha- nisms underlying these paradoxical associations are not clear. A single nucleotide polymorphism in the glucokinase gene, rs1799884, is associated with higher circulating plasma fasting glucose and with an increased risk of type 2 diabetes. We report a case-control study nested within the population-based Prostate testing for cancer and Treatment (ProtecT) study ISRCTN20141297. Men aged 50-69 years based around 9 UK cities were invited for a prostate specific antigen (PSA) test between June 2002 and November 2006. 1,551 cases and 2,993 controls were geno-typed. We observed suggestive evidence for a positive association between the AA variant rs1799884 and PSA-detected prostate cancer (OR(AA V GG)= 1.40, 95% CI= 0.95 to 2.07). There was little evidence that this effect was greater for
TY - JOUR. T1 - The P446L variant in GCKR associated with fasting plasma glucose and triglyceride levels exerts its effect through increased glucokinase activity in liver. AU - Beer, Nicola L.. AU - Tribble, Nicholas D.. AU - McCulloch, Laura J.. AU - Roos, Charlotta. AU - Johnson, Paul R. V.. AU - Orho-Melander, Marju. AU - Gloyn, Anna L.. PY - 2009. Y1 - 2009. N2 - Genome-wide association studies have identified a number of signals for both Type 2 Diabetes and related quantitative traits. For the majority of loci, the transition from association signal to mutational mechanism has been difficult to establish. Glucokinase (GCK) regulates glucose storage and disposal in the liver where its activity is regulated by glucokinase regulatory protein (GKRP; gene name GCKR). Fructose-6 and fructose-1 phosphate (F6P and F1P) enhance or reduce GKRP-mediated inhibition, respectively. A common GCKR variant (P446L) is reproducibly associated with triglyceride and fasting plasma glucose levels in the general ...
As glucokinase patients have mild fasting hyperglycaemia throughout life this often presents during pregnancy when routine testing is performed. Since these patients have a consistently raised fasting blood glucose they will have macrosomic children (as long as their child does not have the mutation). The diagnosis of a glucokinase mutation is important not only as the child may subsequently be picked up as having a raised fasting blood glucose and this may lead to concern about type 1 diabetes but also because the guidelines given to the mother are different from the normal "pre-type 2" diabetic phenotype as they will not deteriorate with time. The following criteria identify when glucokinase testing is appropriate:-. 1. Persistently raised fasting blood glucose in the range of 5.5 - 8 mmol/l both before, during and after pregnancy ...
Basic & Clinical TOPICS 最新論文レビュー 肝臓SIRT2活性の低下が肥満・2型糖尿病モデルでの肝臓糖取り込み障害を引き起こす [in Japanese] Sirt2 facilitates hepatic glucose uptake by deacetylating glucokinase regulatory protein [in Japanese] ...
Monogenic forms of diabetes can be diagnosed at any age. They account for less than 1% of childhood diabetes, but form the majority of cases diagnosed before the ninth month of life. Neonatal diabetes is transient in about half of the cases; if persistent, it presents a significant clinical challenge. Some infants respond better to sulfonylurea than insulin. Maturity-onset diabetes of the young (MODY) presents as a nonketotic and usually non-insulin-dependent diabetes in the absence of obesity or islet autoantibodies. A strong family history of early-onset diabetes is common. The most frequent forms are due to mutations in glucokinase or hepatic nuclear factor 1 or 2 genes. Glucokinase mutations rarely require therapy; other forms respond to oral hypoglycemic agents or insulin. Commercial and research-oriented genotyping services are available to aid correct diagnosis. ...
Cited for: VARIANTS MODY2 GLU-16; ASN-19; PRO-20; TRP-36; SER-43; SER-44; 61-TYR--GLN-465 DEL; SER-61; LYS-70; ARG-72; PRO-77; GLU-78; ASP-80; ILE-82; HIS-108; PRO-116; LEU-182; 186-ARG--GLN-465 DEL; TYR-187; TRP-191; LEU-200; THR-202; MET-206; MET-209; SER-223; ARG-224; SER-227; MET-228; ARG-233; 234-TYR--GLN-465 DEL; GLY-252; ALA-255; LYS-256; ARG-261; LYS-265; LYS-298; TRP-308; HIS-377; VAL-379; LEU-383; 399-GLU--GLN-465 DEL; PHE-411; PRO-416; GLU-420 AND TRP-441; Biochemical characterization of novel glucokinase mutations isolated from Spanish maturity-onset diabetes of the young (MODY2) patients. ...
The present study was undertaken to test the hypothesis that exposure to high glucose concentrations enhances insulin secretion in pancreatic islets from glucokinase-deficient mice. Insulin secretion and intracellular calcium ([Ca2+]i) were measured as the glucose concentration was increased from 2 to 26 mmol/l in islets from heterozygous glucokinase (GK)-deficient mice (GK+/-) and their wild-type littermates (GK+/+). Results obtained in islets incubated in 11.6 or 30 mmol/l glucose for 48-96 h were compared. GK+/- islets that had been incubated in 30 mmol/l glucose showed improved although not normal insulin secretory and [Ca2+]i responses to the standard glucose challenge as well as an enhanced ability to sense small amplitude glucose oscillations. These effects were associated with increased glucokinase activity and protein. In contrast, exposure of GK+/+ islets to 30 mmol/l glucose increased their basal insulin secretion but reduced their incremental secretory responses to glucose and their ...
MK-0941 free base 是具有口服活性的葡糖激酶 (glucokinase) 抑制剂,在葡萄糖浓度为 2.5 和 10 mM 的条件下,对重组人 glucokinase 的 EC50 值分别为 240 和 65 nM。MK-0941 free base 具有较强的降血糖活性,是治疗 2 型糖尿病的候选药物。- 高纯度,全球文献引用。
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Maturity-onset diabetes of the young (MODY) is a genetically and clinically heterogeneous subtype of familial diabetes mellitus characterized by autosomal dominant inheritance, early onset before 25 years of age and primary insulin secretion defects. Mutations in six genes, encoding the glucose sensor enzyme glucokinase and five transcription factors that participate in a regulatory network essential for adult beta cell function, cause most of the MODY cases ...
The expression of some genes controlling energy homeostasis could be regulated by epigenetic mechanisms that may play a role in body weight regulation. Thus, it is known that various nutritional factors affect DNA methylation. In order to assess whether the macronutrient composition of the diet could be related to the epigenetic regulation of gene expression and with obesity development, we investigated the effects on methylation and expression patterns of two pair-fed isocaloric diets in rats: control (rich in starch) and HFS (rich in fat and sucrose). The pair-fed HFS diet induced higher weight gain and adiposity as compared to the controls as well as liver triglyceride accumulation and oxidative stress. Feeding the HFS diet impaired glucose tolerance and serum triglycerides and cholesterol. Liver glucokinase expression, a key glycolytic gene, remained unaltered, as well as the mRNA values of fatty acid synthase and NADH dehydrogenase (ubiquinone) 1 beta subcomplex, 6 (NDUFB6) in liver and visceral
The expression of some genes controlling energy homeostasis could be regulated by epigenetic mechanisms that may play a role in body weight regulation. Thus, it is known that various nutritional factors affect DNA methylation. In order to assess whether the macronutrient composition of the diet could be related to the epigenetic regulation of gene expression and with obesity development, we investigated the effects on methylation and expression patterns of two pair-fed isocaloric diets in rats: control (rich in starch) and HFS (rich in fat and sucrose). The pair-fed HFS diet induced higher weight gain and adiposity as compared to the controls as well as liver triglyceride accumulation and oxidative stress. Feeding the HFS diet impaired glucose tolerance and serum triglycerides and cholesterol. Liver glucokinase expression, a key glycolytic gene, remained unaltered, as well as the mRNA values of fatty acid synthase and NADH dehydrogenase (ubiquinone) 1 beta subcomplex, 6 (NDUFB6) in liver and visceral
There is an epidemic of Type 2 diabetes mostly driven by increasing worldwide obesity and sedentary life style factors [1, 2]. The defining metabolic parameters of Type 2 diabetes are insulin resistance and pancreatic beta cell failure and they are associated with increased rates of cardiovascular disease [3-5]. Existing drugs for the treatment of these factors have thus far been overwhelmed by the pervasive natural history of the disease and no treatment regimens are available which can maintain long term normoglycemia and prevent cardiovascular disease.. The rapid increase in the occurrence of obesity-related Type 2 diabetes commenced in the early 1980s [6]. This event was not fully appreciated by the pharmaceutical industry which in the relevant period and area was concentrating on the development of anti-hypertensive agents; accordingly, there was a large gap in the discovery and introduction of new classes of drugs for the treatment of hyperglycemia. Intense research over the last several ...
Glucokinase (GK) is the central player in glucose-stimulated insulin release from pancreatic b-cells, and catalytic activation by a-D-glucose binding has a key regulatory function. Whereas the mechanism of this activation is well understood, on the basis of crystal structures of human GK, there are no similar structural data on ATP binding to the ligand-free enzyme and how it affects its conformation. ...
Adult, Alleles, Birth Weight/*genetics, Blood Glucose/genetics/*metabolism, England, Female, Genotype, Glucokinase/*genetics, Glucose Intolerance/*genetics, Humans, Islets of Langerhans/*enzymology, Male, Mothers, Polymorphism; Genetic, Promoter Regions (Genetics), Research Support; Non-U.S. Govt, Sweden, Variation (Genetics ...
Buy our Glucokinase peptide. Ab108095 is a blocking peptide for ab37796 and has been validated in BL. Abcam provides free protocols, tips and expert support…
Glucose is phosphorylated to glucose-6-phosphate by glucokinases. This gene is alternatively spliced to generate three different forms of the enzyme; one found in the pan
he action of GRP78/BiP. 1 Proapoptotic Action of a GRP78/BiP Peptidic Ligand Bag-1 is a family of four polypeptides with multifunctional domains that interacts
GCK - GCK (untagged)-Human glucokinase (hexokinase 4) (GCK), transcript variant 3 available for purchase from OriGene - Your Gene Company.
The experiments described here reveal the existence of three serendipitous pathways that allow synthesis of PLP in the ΔpdxB strain when any one of seven different genes is overexpressed. The number of genes that allow complementation is surprising; most multicopy suppression experiments reveal fewer genes that can complement a strain lacking a metabolic enzyme. For example, Patrick et al (2007) found that 21 of 104 knockout strains of E. coli could be complemented by multicopy suppression using the ASKA library, but in most cases by only one or two genes. One exception, the ΔglyA strain, was complemented by four genes, one of which encodes an antisigma factor. A second unusual case was described by Miller and Raines (2004, 2005), who found that overexpression of four genes encoding glycokinases with promiscuous glucokinase activity complemented a strain lacking glucokinase. Our finding that seven different genes complement the ΔpdxB strain is, to our knowledge, the record. Furthermore, our ...
The PDB archive contains information about experimentally-determined structures of proteins, nucleic acids, and complex assemblies. As a member of the wwPDB, the RCSB PDB curates and annotates PDB data according to agreed upon standards. The RCSB PDB also provides a variety of tools and resources. Users can perform simple and advanced searches based on annotations relating to sequence, structure and function. These molecules are visualized, downloaded, and analyzed by users who range from students to specialized scientists.
The PDB archive contains information about experimentally-determined structures of proteins, nucleic acids, and complex assemblies. As a member of the wwPDB, the RCSB PDB curates and annotates PDB data according to agreed upon standards. The RCSB PDB also provides a variety of tools and resources. Users can perform simple and advanced searches based on annotations relating to sequence, structure and function. These molecules are visualized, downloaded, and analyzed by users who range from students to specialized scientists.
And fourth, limiting sugar consumption is not the only line of defense for preventing and reversing cancer. In fact, a botanical extract from the avocado plant is showing promise as a new cancer adjunct. When a purified avocado extract was added to a number of tumor cell lines tested in vitro by researchers in the Department of Biochemistry at Oxford University in Britain, they found it inhibited tumor cell glucose uptake by 25 to 75 percent, and it inhibited the enzyme glucokinase responsible for glycolysis. It also inhibited the growth rate of the cultured tumor cell lines.. YOU CAN PREVENT ALZHEIMERS, ADD/ADHT, DEPRESSION, AND VIOLENCE:. Scientists in the US have now shown a definite link between excess levels of homocysteine, an intermediate component in the synthesis of the amino acid cysteine, and the shrinkage of the brain in middle age, which often later leads to Alzheimers.. This has prompted the astounding declaration that a simple course of vitamins and minerals could prevent a ...
Diabetes is a disorder characterized by loss of β cell mass and/or β cell function, leading to deficiency of insulin relative to metabolic need. To determine whether stem cell-derived β cells recapitulate molecular-physiological phenotypes of a diabetic subject, we generated induced pluripotent stem cells (iPSCs) from subjects with maturity-onset diabetes of the young type 2 (MODY2), which is characterized by heterozygous loss of function of the gene encoding glucokinase ...
3h1v: The design and optimization of a series of 2-(pyridin-2-yl)-1H-benzimidazole compounds as allosteric glucokinase activators.
A variety of stressful conditions, such as heat shock, ethanol, osmotic shock, glucose deprivation, and oxidative stress, are known to induce the synthesis of specific proteins. Here, we report the induction in Escherichia coli of a protein elicited in response to a hitherto unidentified stress cond …
InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites. We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their individual strengths to produce a powerful integrated database and diagnostic tool.
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class="publication">Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href="http://www.nrbook.com/b/bookcpdf.php">Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
cdu:CD36_32740 K00844 hexokinase [EC:2.7.1.1] , (RefSeq) glucokinase, putative (A) MSLSPKLEETVSSIEKAFDIKDDFLVKATEYFIESMNVGLESPKPSKDVMPMIPTYVTSI PTGKEVGLYLAADLGGTNFRVCSIDLKGDHTFTMKQSKYRLPVDLMKAEKSDDLFSFLAK KVQSFLLEHHSEACSAKNAEPLKLGFTFSFPVNQTALDRGTLIRWTKGFDIPDAVDRDVV ELLQANLTVLEVNVKVVAIANDTVGTLLTAAYSNDPEKTNRNTIIGCIFGTGTNGAYFES KIPKLASSKGMVINTEWGSFDNGLKILPCTEFDKIVDSETANPGYHLFEKRISGMFLGEI LRVVLINLFEKGLIFQELYKARGGSLPHRIQEPWLLDAEVLSYLQIDDSTDLRMSGLILQ NVLRLETNKEERVVIQRLTRAISKRAAHLSAIPIAAIAKKVKDQYKDDDRDFEVGCDGSV VEFYPGFRQAVLESVEKINPLKGTNKKIYLKIAKDGSGVGAALCASTA ...
GK2兔多克隆抗体(ab96818)可与人样本反应并经WB, ICC/IF实验严格验证。中国75%以上现货,所有产品均提供质保服务,可通过电话、电邮或微信获得本地专属技术支持。
Falkum, T., Konnerup-Madsen, J. & Rose-Hansen, J., 1985, The Deep Proterozoic Crust in the North Atlantic Provinces. Tobi, A. S. C. & Touret, J. L. R. (red.). D. Reidel Publishing Group, s. 579-583 Publikation: Bidrag til bog/antologi/rapport › Bidrag til bog/antologi › Forskning ...