ELISA/assay

Rat HbA1C (Glycosylated Hemoglobin/Hemoglobin A1c) ELISA Kit

MBS2509196

48-Strip-Wells

430 USD

ELISA Kit

Rat HbA1C (Glycosylated Hemoglobin/Hemoglobin A1c) ELISA Kit

HbA1C

hemoglobin subunit alpha; Hemoglobin subunit alpha; hemoglobin subunit alpha; alpha one globin; alpha-1 globin; alpha-1-globin; alpha-2 globin chain; alpha-globin; delta globin; hemoglobin alpha 1 globin chain; hemoglobin alpha chain; hemoglobin alpha-1 chain; hemoglobin, alpha 1; Alpha-globin; Hemoglobin alpha chain

HbA1c

HBA1; HBA1; HBH; HBA-T3

HBA_HUMAN

Rat

142

This kit recognizes natural and recombinant Rat HbA1c. No significant cross-reactivity or interference between Rat HbA1c and analogues was observed.

Store at 4 degree C.

Samples: Serum, plasma and other biological fluids. Assay Type: Sandwich. Detection Range: 1.563-100ng/mL. Sensitivity: The minimum detectable dose of Rat HbA1c is 0.938ng/mL

Intended Uses This ELISA kit applies to the in vitro quantitative determination of Rat HbA1c concentrations in serum, plasma and other biological fluids. Principle of the Assay: This ELISA kit uses Sandwich-ELISA as the method. The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to HbA1c. Standards or samples are added to the appropriate micro ELISA plate wells and combined with the specific antibody. Then a biotinylated detection antibody specific for HbA1c and Avidin-Horseradish Peroxidase (HRP) conjugate is added to each micro plate well successively and incubated. Free components are washed away. The substrate solution is added to each well. Only those wells that contain HbA1c, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. The enzyme-substrate reaction is terminated by the addition of a sulphuric acid solution and the color turns yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 nm +/- 2 nm. The OD value is proportional to the concentration of HbA1c. You can calculate the concentration of HbA1c in the samples by comparing the OD of the samples to the standard curve.

4504347

NP_000549.1

NM_000558.4

P69905

15,258 Da

African Trypanosomiasis Pathway (194384); African Trypanosomiasis Pathway (194323); Binding And Uptake Of Ligands By Scavenger Receptors Pathway (771599); Erythrocytes Take Up Carbon Dioxide And Release Oxygen Pathway (645347); Erythrocytes Take Up Oxygen And Release Carbon Dioxide Pathway (645348); Malaria Pathway (152665); Malaria Pathway (152657); Metabolism Pathway (477135); O2/CO2 Exchange In Erythrocytes Pathway (645346); Scavenging Of Heme From Plasma Pathway (771600)

The human alpha globin gene cluster located on chromosome 16 spans about 30 kb and includes seven loci: 5'- zeta - pseudozeta - mu - pseudoalpha-1 - alpha-2 - alpha-1 - theta - 3'. The alpha-2 (HBA2) and alpha-1 (HBA1) coding sequences are identical. These genes differ slightly over the 5' untranslated regions and the introns, but they differ significantly over the 3' untranslated regions. Two alpha chains plus two beta chains constitute HbA, which in normal adult life comprises about 97% of the total hemoglobin; alpha chains combine with delta chains to constitute HbA-2, which with HbF (fetal hemoglobin) makes up the remaining 3% of adult hemoglobin. Alpha thalassemias result from deletions of each of the alpha genes as well as deletions of both HBA2 and HBA1; some nondeletion alpha thalassemias have also been reported. [provided by RefSeq, Jul 2008]

HBA1: Involved in oxygen transport from the lung to the various peripheral tissues. Defects in HBA1 may be a cause of Heinz body anemias (HEIBAN). This is a form of non-spherocytic hemolytic anemia of Dacie type 1. After splenectomy, which has little benefit, basophilic inclusions called Heinz bodies are demonstrable in the erythrocytes. Before splenectomy, diffuse or punctate basophilia may be evident. Most of these cases are probably instances of hemoglobinopathy. The hemoglobin demonstrates heat lability. Heinz bodies are observed also with the Ivemark syndrome (asplenia with cardiovascular anomalies) and with glutathione peroxidase deficiency. Defects in HBA1 are the cause of alpha-thalassemia (A- THAL). The thalassemias are the most common monogenic diseases and occur mostly in Mediterranean and Southeast Asian populations. The hallmark of alpha-thalassemia is an imbalance in globin-chain production in the adult HbA molecule. The level of alpha chain production can range from none to very nearly normal levels. Deletion of both copies of each of the two alpha-globin genes causes alpha(0)-thalassemia, also known as homozygous alpha thalassemia. Due to the complete absence of alpha chains, the predominant fetal hemoglobin is a tetramer of gamma-chains (Bart hemoglobin) that has essentially no oxygen carrying capacity. This causes oxygen starvation in the fetal tissues leading to prenatal lethality or early neonatal death. The loss of three alpha genes results in high levels of a tetramer of four beta chains (hemoglobin H), causing a severe and life-threatening anemia known as hemoglobin H disease. Untreated, most patients die in childhood or early adolescence. The loss of two alpha genes results in mild alpha-thalassemia, also known as heterozygous alpha-thalassemia. Affected individuals have small red cells and a mild anemia (microcytosis). If three of the four alpha-globin genes are functional, individuals are completely asymptomatic. Some rare forms of alpha-thalassemia are due to point mutations (non- deletional alpha-thalassemia). The thalassemic phenotype is due to unstable globin alpha chains that are rapidly catabolized prior to formation of the alpha-beta heterotetramers. Alpha(0)-thalassemia is associated with non-immune hydrops fetalis, a generalized edema of the fetus with fluid accumulation in the body cavities due to non-immune causes. Non- immune hydrops fetalis is not a diagnosis in itself but a symptom, a feature of many genetic disorders, and the end-stage of a wide variety of disorders. Defects in HBA1 are the cause of hemoglobin H disease (HBH). HBH is a form of alpha-thalassemia due to the loss of three alpha genes. This results in high levels of a tetramer of four beta chains (hemoglobin H), causing a severe and life-threatening anemia. Untreated, most patients die in childhood or early adolescence. Belongs to the globin family. Protein type: Carrier. Chromosomal Location of Human Ortholog: 16p13.3. Cellular Component: membrane; hemoglobin complex; extracellular region; cytosol. Molecular Function: haptoglobin binding; protein binding; peroxidase activity; iron ion binding; heme binding; oxygen binding; oxygen transporter activity. Biological Process: receptor-mediated endocytosis; response to hydrogen peroxide; protein heterooligomerization; oxygen transport; hydrogen peroxide catabolic process; bicarbonate transport. Disease: Hemoglobin H Disease; Heinz Body Anemias; Alpha-thalassemia

48-Strip-Wells

430 USD

96-Strip-Wells

520