type 2 diabetes

Confers resistance to the different beta-lactams antibiotics (penicillin, cephalosporin and carbapenem) via the hydrolysis of the beta-lactam ring. Metallo-beta-lactamase type 2 Protein, Serratia marcescens, Recombinant (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 32.6 kDa and the accession number is P52699.

Dengue virus (DENV) (type 2, strain New Guinea C) NS1 Protein (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 42.3 kDa and the accession number is AAC59275.1.

Dengue virus (DENV) (type 2, strain New Guinea C/PUO-218 hybrid) E/Envelope Protein (aa 247-675, His) is expressed in Baculovirus insect cells with His tag. The predicted molecular weight is 49.2 kDa and the accession number is AAC59274.1.

Staphylococcal enterotoxin that activates the host immune system by binding as unprocessed molecules to major histocompatibility (MHC) complex class II and T-cell receptor (TCR) molecules. In turn, this ternary complex activates a large number of T-lymphocytes initiating a systemic release of proinflammatory cytokines. Causes also the intoxication staphylococcal food poisoning syndrome. Enterotoxin type C-2 Protein, S. aureus, Recombinant is expressed in E. coli expression system. The predicted molecular weight is 27.6 kDa and the accession number is P34071.

Dengue virus (DENV) (type 2, strain New Guinea C/PUO-218 hybrid) E/Envelope Protein (aa 281-679, T76R,Q77E,W101R,L107R,His) is expressed in Baculovirus insect cells with His tag. The predicted molecular weight is 45.7 kDa and the accession number is AAC59274.1.

Canine parvovirus type 2 (CPV-2) VP2 Protein (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 65.9 kDa and the accession number is P61826.

Confers resistance to the different beta-lactams antibiotics (penicillin, cephalosporin and carbapenem) via the hydrolysis of the beta-lactam ring. Does not confer resistance to the polymixin colistin or the fluoroquinolone ciprofloxacin.

Staphylococcal enterotoxin that activates the host immune system by binding as unprocessed molecules to major histocompatibility (MHC) complex class II and T-cell receptor (TCR) molecules. In turn, this ternary complex activates a large number of T-lymphocytes initiating a systemic release of proinflammatory cytokines. Causes also the intoxication staphylococcal food poisoning syndrome. Enterotoxin type C-2 Protein, S. aureus, Recombinant (His & SUMO) is expressed in E. coli expression system with N-6xHis-SUMO tag. The predicted molecular weight is 43.6 kDa and the accession number is P34071.

Dengue virus (DENV) (type 2, strain New Guinea C/PUO-218 hybrid) E/Envelope Protein (aa 578-680, His) is expressed in yeast with His tag. The predicted molecular weight is 13 kDa and the accession number is AAC59274.1.

Collagen alpha-1(VIII) chain, also known as endothelial collagen, C3orf7 and COL8A1, can be cleaved into vastatin chain. COL8A1 is a short chain collagen and a major component of the basement membrane of the corneal endothelium. COL8A1 forms homotrimers, or heterotrimers in association with alpha 2(VIII) type collagens. Four homotrimers can form a tetrhedron stabilized by central interacting C-terminal NC1 trimers. COL8A1 contains one C1q domain and is primarily expressed in the subendothelium of large blood vessels. The expression level can be up-regulated during vascular injury, in atherosclerosis and in diabetes. COL8A1 may have a role in the maintenance of vessel wall integrity and structure, in particular in atherogenesis.

ADGRG1 (Adhesion G Protein-Coupled Receptor G1, also known as GPR56) is a Protein Coding gene. GPR56 is a member of an adhesion G protein-coupled receptor family with a very long N-terminal stalk and seven transmembrane domains. The encoded protein binds specifically to transglutaminase 2, a component of tissue and tumor stroma implicated as an inhibitor of tumor progression. GPR56 may be a target for the treatment of type 2 diabetes. GPR56 inhibits melanoma metastatic growth by impeding the expansion of micrometastases to macrometastases. GPR56 loss of function promotes mesenchymal differentiation and radioresistance of glioma initiating cells both in vitro and in vivo. Diseases associated with ADGRG1 include Polymicrogyria, Bilateral Frontoparietal, and Polymicrogyria, Bilateral Perisylvian, Autosomal Recessive.

SerpinB1 is an endogenous inhibitor of serine proteases recognized for its anti-inflammatory and host-protective properties. Serum SerpinB1 levels are elevated in patients with type 2 diabetes compared with that in healthy subjects and are negatively correlated with serum LDL-C. serpinB1 as an endogenous protein that can potentially be harnessed to enhance functional beta cell mass in patients with diabetes.

Mitogen-activated protein kinase 8 (MAPK8), also known as JNK1, is a member of the MAP kinase family. MAP kinases act as an integration point for multiple biochemical signals and are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation, and development. The protein kinases JNK1 has been found to serve as critical molecular links between obesity, metabolic inflammation, and disorders of glucose homeostasis. It is critically involved in the promotion of diet-induced obesity, metabolic inflammation, and beta-cell dysfunction. The selective deficiency of JNK1 in the murine nervous system is sufficient to suppress diet-induced obesity. Genetic analysis indicates that the effects of JNK1 can be separated from the effects of JNK1 on obesity. JNK1 is a potential pharmacological target for the development of drugs that might be useful for the treatment of metabolic syndrome, and type 2 diabetes. Furthermore, JNK1 plays a major role in hypoxic cellular damage. JNK1 protein might be an attractive target for anti-hypoxic therapy in increasing resistance to many pathological conditions and diseases, leading to the oxygen deficit.

Her4, a member of the EGF receptor family, plays a variety of roles in physiological and pathological states. Genetic studies have indicated a link between Her4 and type 2 diabetes and obesity. Her4 may play an important role in glucose homeostasis and lipogenesis. Her4 deficiency-related obesity and adipose tissue inflammation may contribute to the development of MetS. HER4/ERBB4 Protein, Human, Recombinant (His & Avi) is expressed in HEK293 mammalian cells with C-His-Avi tag. The predicted molecular weight is 72.7 kDa and the accession number is Q15303-1.

ILDR2 is a member of the B7-like family of proteins that regulate T cell activity, is also a known endoplasmic reticulum molecule that regulates lipid homeostasis. The human ILDR2 lumenal domain shares a 99% and 98% homology with the mouse and rat respectively. The human gene encoding ILDR2 is located in a region on Chr1q23–25 that has been associated with type 2 diabetes. ILDR2 plays critical roles in hepatic clearance of lipoproteins and in lipid homeostasis. ILDR2 regulates human dendritic cells (DC2 cells, a subpopulation of polarized DCs that promotes Th2 differentiation). Recent publications reported that ILDR2 displayed negative regulatory functions on human and mouse T cells in various experimental systems. Fusion protein of ILDR2 lumenal domain with an Fc fragment, displays therapeutic effects in collagen-induced arthritis (CIA), a mouse model of rheumatoid arthritis (RA). ILDR2 represents a novel B7-like ligand that exerts negative immune modulation via interaction with a putative counterpart receptor expressed on activated T cells.

Class-I Restricted T Cell-Associated Molecule (CRTAM) is a protein that is expressed after T cell activation. The interaction of CRTAM with its ligand, nectin-like 2 (Necl2), is required for the efficient production of IL-17, IL-22, and IFNγ by murine CD4 T cells, and it plays a role in optimal CD8 T and NK cell cytotoxicity. CRTAM promotes the pro-inflammatory cytokine profile; therefore, it may take part in the immunopathology of autoimmune diseases such as diabetes type 1 or colitis. CRTAM Protein, Mouse, Recombinant (His) is expressed in HEK293 mammalian cells with C-His tag. The predicted molecular weight is 31.1 kDa and the accession number is Q149L7-1.

Her4, a member of the EGF receptor family, plays a variety of roles in physiological and pathological states. Genetic studies have indicated a link between Her4 and type 2 diabetes and obesity. Her4 may play an important role in glucose homeostasis and lipogenesis. Her4 deficiency-related obesity and adipose tissue inflammation may contribute to the development of MetS. HER4/ERBB4 Protein, Human, Recombinant (His & Avi), Biotinylated is expressed in HEK293 mammalian cells with C-His-Avi tag. The predicted molecular weight is 72.7 kDa and the accession number is Q15303-1.

SMAD3 belongs to the SMAD family. Members of this family mediate signal transduction by the TGF-beta/activin/BMP-2/4 cytokine superfamily from receptor Ser/Thr protein kinases at the cell surface to the nucleus. SMAD3 is involved in cell signalling. It modulates signals of activin and TGFβ's. Binding of SMAD3 with SMAD4 enables its transmigration into the nucleus where it forms complexes with other proteins and acts as a transcription factor. SMAD3 is a receptor-regulated SMAD (R-SMAD). In mice, mutation of SMAD3 has been linked to colorectal adenocarcinoma, increased systemic inflammation, and accelerated wound healing. Increased SMAD3 activity has been implicated in the pathogenesis of scleroderma. Smad3 is also a multifaceted regulator in adipose physiology and the pathogenesis of obesity and type 2 diabetes.

Erythropoietin (EPO) is a glycoprotein hormone that is principally known for its role in erythropoiesis, where it is responsible for stimulating proliferation and differentiation of erythroid progenitor cells. Erythropoietin is a member of the EPO/TPO family. It is a secreted, glycosylated cytokine composed of four alpha helical bundles. The differentiation of CFU-E (Colony Forming Unit-Erythroid) cells into erythrocytes can only be accomplished in the presence of EPO. Physiological levels of EPO in adult mammals are maintained primarily by the kidneys, whereas levels in fetal or neonatal mammals are maintained by the liver. EPO also can exert various non-hematopoietic activities, including vascularization and proliferation of smooth muscle, neural protection during hypoxia, and stimulation of certain B cells. Genetic variation in erythropoietin is associated with susceptbility to microvascular complications of diabetes type 2. These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy.

Insulin-Like Growth Factor 2 mRNA-Binding Protein 2 (IGFBP2) belongs to the RRM IMP/VICKZ family. IGFBP2 is a cytoplasmic protein and contains four KH domains and two RRM (RNA recognition motif) domains. IGF2BP2 binds to the 5'-UTR of the Insulin-Like Growth Factor 2 (IGF2) mRNA. This binding is isoform-specific. IGF2BP2 may regulate translation of target mRNAs. Genetic variation at the IGF2BP2 gene has been associated with type 2 diabetes (T2D) by genome-wide association studies and by replication analyses.

Astrocyticphosphoprotein PEA-15 (PEA15) is a death effector domain (DED)-containing protein. PEA15 is mainly expressed in the central nervous system, principally in astrocytes. Increased PEA15 levels affect tumorigenesis and cancer progression. PEA15 is overexpressed in breast cancers and gliomas as well as in type 2 diabetes. PEA15 blocks Ras-mediated inhibition of integrin activation and modulates the ERK MAP kinase cascade. PEA15 also inhibits RPS6KA3 activities by holding it in the cytoplasm. In addition, PEA15 inhibits both TNFRSF6 and TNFRSF1A mediated CASP8 activity and apoptosis. At present, PEA15 expression is also a significant prognostic marker in ovarian cancer.

Class-I Restricted T Cell-Associated Molecule (CRTAM) is a protein that is expressed after T cell activation. The interaction of CRTAM with its ligand, nectin-like 2 (Necl2), is required for the efficient production of IL-17, IL-22, and IFNγ by murine CD4 T cells, and it plays a role in optimal CD8 T and NK cell cytotoxicity. CRTAM promotes the pro-inflammatory cytokine profile; therefore, it may take part in the immunopathology of autoimmune diseases such as diabetes type 1 or colitis. CRTAM Protein, Canine, Recombinant (His) is expressed in HEK293 mammalian cells with C-His tag. The predicted molecular weight is 31.19 kDa and the accession number is E2QWY2.

The potential application of glucose-dependent insulinotropic polypeptide (gastric inhibitory polypeptide, GIP) in the management of obesity and type 2 diabetes has been controversial. Initial interest in the therapeutic use of GIP was dampened by evidence that its insulinotropic activity was reduced in type 2 diabetes and by reports that it increased glucagon secretion and adipose deposition in non-diabetic individuals. GIP Protein, Mouse, Recombinant (hFc) is expressed in HEK293 mammalian cells with C-hFc tag. The predicted molecular weight is 34.3 kDa and the accession number is P48756.

The potential application of glucose-dependent insulinotropic polypeptide (gastric inhibitory polypeptide, GIP) in the management of obesity and type 2 diabetes has been controversial. Initial interest in the therapeutic use of GIP was dampened by evidence that its insulinotropic activity was reduced in type 2 diabetes and by reports that it increased glucagon secretion and adipose deposition in non-diabetic individuals. GIP Protein, Mouse, Recombinant (His) is expressed in HEK293 mammalian cells with C-His tag. The predicted molecular weight is 8.7 kDa and the accession number is P48756.

The potential application of glucose-dependent insulinotropic polypeptide (gastric inhibitory polypeptide, GIP) in the management of obesity and type 2 diabetes has been controversial. Initial interest in the therapeutic use of GIP was dampened by evidence that its insulinotropic activity was reduced in type 2 diabetes and by reports that it increased glucagon secretion and adipose deposition in non-diabetic individuals. GIP Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with C-His tag. The predicted molecular weight is 9.2 kDa and the accession number is P09681.

Fatty acid binding protein (FABP) is one of the intracellular proteins, with a low molecular weight of approximately 15 kDa, that plays important roles in the transportation and metabolism of long-chain fatty acids. FABP family proteins could be used as tissue specific injury marker based on the following characteristics of FABP. The intestinal fatty acid binding protein (I-FABP), or fatty acid-binding protein 2 (FABP2), an intracellular protein expressed only in the intestine, involved in the absorption and intracellular transport of dietary long chain fatty acids. The FABP2 gene is proposed as a candidate gene for diabetes because the protein it codes is involved in fatty acid (FA) absorption and metabolism. Numerous studies have assessed FABP2 gene variants. A transition of G to A at codon 54 of FABP2 results in an amino acid substitution (Ala54 to Thr54), which is common in diverse populations and results in increased FA absorption in vivo. Some evidence indicates that this variant may be associated with type 2 diabetes. This polymorphism was associated with some cardiovascular risk factors. The cytosolic human intestinal fatty acid binding protein (hFABP2) is proposed to be involved in intestinal absorption of long-chain fatty acids. FABP2 may also help maintain energy homeostasis by functioning as a lipid sensor.

Glucokinase belongs to the bacterial glucokinase family. Hexokinases 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). It can Catalyzes the initial step in utilization of glucose by the beta-cell and liver at physiological glucose concentration. Glucokinase has a high Km for glucose, and so it is effective only when glucose is abundant. The role of GCK is to provide G6P for the synthesis of glycogen. Pancreatic glucokinase plays an important role in modulating insulin secretion. Hepatic glucokinase helps to facilitate the uptake and conversion of glucose by acting as an insulin-sensitive determinant of hepatic glucose usage. It has a pivotal role as glucose sensor of the pancreatic beta-cells. Glucokinase explains the capacity, hexose specificity, affinities, sigmoidicity, and anomeric preference of pancreatic islet glycolysis, and because stimulation of glucose metabolism is a prerequisite of glucose stimulation of insulin release, glucokinase also explains many characteristics of this beta-cell function. Glucokinase of the beta-cell is induced or activated by glucose in contrast to liver glucokinase, which is regulated by insulin. Tissue-specific regulation corresponds with observations that liver and pancreatic beta-cell glucokinase are structurally distinct. Glucokinase could play a glucose-sensor role in hepatocytes as well, and certain forms of diabetes mellitus might be due to glucokinase deficiencies in pancreatic beta-cells, hepatocytes, or both.