产品介绍
糖尿病分子标志物检测试剂盒
货号: BR-1103D 规格: 96 Assay 价格: ￥3926.00
Diabetes Mellitus Molecular Marker (INSR and GCK) Detection Kit
Description: The kit provides a means of performing Diabetes Mellitus detection method based on kinase activity assays. Three targets of molecular marker (INSR and GCK) are involved in Diabetes Mellitus. This kit includes Streptavidin Coated Plates and specific Substrate-Peptides (biotinylated peptide substrates) for detection of the activity of INSR and GCK which indicate the prognosis of Diabetes Mellitus.
Molecular Markers in Diabetes Mellitus
|
Disease
|
Molecular Marker
|
Gene ID
|
Gene Disease Relation
|
|
Diabetes Mellitus
|
INSR
|
3643
|
marker/mechanism
|
|
Diabetes Mellitus
|
INSR
|
3643
|
marker/mechanism
|
|
Diabetes Mellitus
|
GCK
|
2645
|
marker/mechanism
|
- Molecular markers for drug discovery and life science research (mechanism).
Peptide Core Sequence:
Specific Substrate-Peptides for Diabetes Mellitus Molecular Marker
|
Molecular Marker
|
Substrate-Peptide
|
Active Residue
|
Reaction Type
|
|
INSR
|
Peptides Mix
|
Tyr-628
|
Phosphorylation
|
|
INSR
|
Peptides Mix
|
Tyr-132
|
Phosphorylation
|
|
GCK
|
Peptides Mix
|
Tyr- 6
|
Phosphorylation
|
Label of Substrate-Peptides: Biotinylated.
Quality Control: The substrate peptide was selected using our Diabetes Mellitus Diagnosis Kit. The quality of the biotinylated peptide was evaluated by reverse-phase HPLC and by mass spectrometry.
Storage:
Store at 4 °C, Avoid Freeze.
Background:
INSR is activated by insulin. It belongs to the large class of tyrosine kinase receptors. Two alpha subunits and two beta subunits make up the insulin receptor. The beta subunits pass through the cellular membrane and are linked by disulfide bonds. The alpha and beta subunits are encoded by a single gene (INSR). The insulin receptor has also recently been designated CD220. Tyrosine kinase receptors, including the insulin receptor, mediate their activity by causing the addition of a phosphate group to particular tyrosines on certain proteins within a cell. The "substrate" proteins that are phosphorylated by the Insulin Receptor include a protein called "IRS-1" for "insulin receptor substrate 1". IRS-1 binding and phosphorylation eventually leads to an increase in the high affinity glucose transporter (Glut4) molecules on the outer membrane of insulin-responsive tissues, including muscle cells and adipose tissue, and therefore to an increase in the uptake of glucose from blood into these tissues. In other words, the glucose transporter Glut4 is transported from cellular vesicles to the cell surface, where it then can mediate the transport of glucose into the cell. The main activity of activation of the insulin receptor is inducing glucose uptake. For this reason "insulin insensitivity", or a decrease in insulin receptor signaling, leads to diabetes mellitus type 2 – the cells are unable to take up glucose, and the result is hyperglycemia (an increase in circulating glucose), and all the sequelae that result from diabetes. Patients with insulin resistance may display acanthosis nigricans. A few patients with homozygous mutations in the INSR gene have been described, which causes Donohue syndrome or Leprechaunism. This autosomal recessive disorder results in a totally non-functional insulin receptor. These patients have low-set, often protuberant, ears, flared nostrils, thickened lips, and severe growth retardation. In most cases, the outlook for these patients is extremely poor, with death occurring within the first year of life. Other mutations of the same gene cause the less severe Rabson-Mendenhall syndrome, in which patients have characteristically abnormal teeth, hypertrophic gingiva (gums), and enlargement of the pineal gland. Both diseases present with fluctuations of the glucose level: After a meal the glucose is initially very high, and then falls rapidly to abnormally low levels. GCK phosphorylate glucose to produce glucose-6-phosphate, the first step in most glucose metabolism pathways. Alternative splicing of this gene results in three tissue-specific forms of glucokinase, one found in pancreatic islet beta cells and two found in liver. The protein localizes to the outer membrane of mitochondria. In contrast to other forms of hexokinase, this enzyme is not inhibited by its product glucose-6-phosphate but remains active while glucose is abundant. Mutations in this gene have been associated with non-insulin dependent diabetes mellitus (NIDDM), maturity onset diabetes of the young, type 2 (MODY2) and persistent hyperinsulinemic hypoglycemia of infancy (PHHI).
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