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I-GLK (Glucokinase isoform 2)
Purification and Quality Control
The His-tag recombinant protein is purified by affinity chromatography in combination with FPLC columns.
The purified I-GLK (isoform 2) is greater than 95% homogeneous based on SDS-PAGE analysis.
Unit Definition (Activity)
1 unit equals 1 nanogram of purified protein.
Applications
GLK may be used for the phosphorylation of glucose. For Research Use Only.
Formulation and Storage
The protein is in 20mM Tris-HCl pH7.9,100mM NaCl, 0.2mM EDTA, 1mM DTT and 20% glycerol. Stored at -70°C before use. Avoid repeated freeze thaw cycles.
Synonym
homo sapiens glucokinase (hexokinase 4) (GCK), transcript variant 2; FGQTL3; GK; GLK; HHF3; HK4; HKIV; HXKP; LGLK and MODY2.
Protein Sequence
MAMDVTRSQA QTALTLVEQI LAEFQLQEED LKKVMRRMQK EMDRGLRLET HEEASVKMLP
TYVRSTPEGS EVGDFLSLDL GGTNFRVMLV KVGEGEEGQW SVKTKHQMYS IPEDAMTGTA
EMLFDYISEC ISDFLDKHQM KHKKLPLGFT FSFPVRHEDI DKGILLNWTK GFKASGAEGN
NVVGLLRDAI KRRGDFEMDV VAMVNDTVAT MISCYYEDHQ CEVGMIVGTG CNACYMEEMQ
NVELVEGDEG RMCVNTEWGA FGDSGELDEF LLEYDRLVDE SSANPGQQLY EKLIGGKYMG
ELVRLVLLRL VDENLLFHGE ASEQLRTRGA FETRFVSQVE SDTGDRKQIY NILSTLGLRP
STTDCDIVRR ACESVSTRAA HMCSAGLAGV INRMRESRSE DVMRITVGVD GSVYKLHPSF
KERFHASVRR LTPSCEITFI ESEEGSGRGA ALVSAVACKK ACMLGQ
Background
Glucokinase, also termed Hexokinase D, is the characteristic isoenzyme of hexokinase in pancreatic islet ß-cells (IGLK, B-type GK; GKB) and in the liver (L-Type GK; GKL) that phosphorylates glucose at the sixth carbon position, thus committing glucose to the glycolytic pathway (1). The protein localizes to the outer membrane of mitochondria. In contrast with other forms of hexokinase, GK is not inhibited by its product (glucose-6-phosphate) but remains active while glucose is abundant. In B-type GK-containing cells, glucose is the predominant inducer of GK(2). Glucose-driven GK expression is modified by many positive and negative factors: it is augmented by cAMP, biotin, retinoic acid, PL, and insulin, and it is decreased by low cytosolic Ca2+ levels. Even though insulin is not sufficient to induce the enzyme, the hormone may still be required for optimal GK expression in B-type GK-containing cells (reviewed in 3). To date, over 150 GK gene mutations have been found that are manifest in at least three clearly distinguishable syndromes inherited in an autosomal dominant manner: 1) GK-linked persistent hyperinsulinemic hypoglycemia (PHHI-GK) (4); 2) GK-linked permanent neonatal diabetes (PNDM-GK) (5); and 3) GK-linked maturity- onset diabetes of the young (MODY-GK, also called MODY-2) (6). Recently, a novel class of drugs that stimulate the GK molecule directly have been discovered (7), which offer a new principle for drug therapy of diabetes.
References
1. Bell GI, et al., 2002 Enc of Mol Med., p.1437 –1442
2. Liang Y, et al., 1992 Diabetes 41, 792 –806
3. Matchinsky, FM 2002, Diabetes 51, S394-S404
4. Glaser B, et al., 1998 N Engl J Med 338, 226 –230
5. Njolstad PR, et al., 2001. N Engl J Med 344, 1588 –1592
6. Froguel P, et al., 1993 N Engl J Med 328, 697 –702
7. Grimsby J, et al., 2001 Diabetes 50 (Suppl. 2), A115
This products is recommended For RESEARCH USE ONLY and is Not qualified for Use in Diagnostic or Therapeutic Procedures.
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