Key features and details
- HRP Goat polyclonal to Hemoglobin
- Suitable for: WB
- Reacts with: Human
- Conjugation: HRP
- Isotype: IgG
Product nameHRP Anti-Hemoglobin antibody
See all Hemoglobin primary antibodies
DescriptionHRP Goat polyclonal to Hemoglobin
SpecificityThe antibody has been tested in ELISA and IEP with a Human Hemaglobin Calibrator/Standard but has yet to be tested against endogenous protein.
Tested applicationsSuitable for: WBmore details
Species reactivityReacts with: Human
Predicted to work with: Rabbit, Dog, Chimpanzee, Rhesus monkey
Full length protein corresponding to Human Hemoglobin conjugated to bovine serum albumin. Goats were immunized with purified human hemoglobin A1 of adult red blood cell origin.
- recombinant human hemoglobin
Molar enzyme/antibody protein ratio is 4:1.
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Storage instructionsShipped at 4°C. Store at +4°C.
Storage bufferpH: 6.8
Preservative: 0.01% Thimerosal (merthiolate)
Constituents: 1.19% HEPES, 0.58% Sodium chloride
Concentration information loading...
PurityImmunogen affinity purified
Purification notesAntibody concentration was determined by extinction coefficient prior to conjugation: absorbance at 280 nm of 1.4 equals 1.0 mg of IgG.
- TMB ELISA Substrate (Highest Sensitivity) (ab171522)
- TMB ELISA Substrate (High Sensitivity) (ab171523)
- TMB ELISA Substrate (Fast Kinetic Rate) (ab171524)
- TMB ELISA Substrate (Slow Kinetic Rate) (ab171525)
- TMB ELISA Substrate (Slower Kinetic Rate) (ab171526)
- TMB ELISA Substrate (Slowest Kinetic Rate) (ab171527)
- 450 nm Stop Solution for TMB Substrate (ab171529)
- 650 nm Stop Solution for TMB Substrate (ab171531)
- Immunoassay Blocking Buffer (ab171534)
- Immunoassay Blocking (BSA Free) (ab171535)
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab19362 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
1/1000 - 1/30000. Predicted molecular weight: 16 kDa.
1/1000 - 1/30000. Predicted molecular weight: 16 kDa.
FunctionInvolved in oxygen transport from the lung to the various peripheral tissues.
Tissue specificityRed blood cells.
Involvement in diseaseDefects in HBA1/HBA2 may be a cause of Heinz body anemias (HEIBAN) [MIM:140700]. 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/HBA2 are the cause of alpha-thalassemia (A-THAL) [MIM:604131]. 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.
Note=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.
Sequence similaritiesBelongs to the globin family.
modificationsThe initiator Met is not cleaved in variant Thionville and is acetylated.
- Information by UniProt
- 3-prime alpha-globin gene antibody
- A gamma globin antibody
- Alpha 1 globin antibody
ab19362 has been referenced in 4 publications.
- Posta N et al. Hemoglobin oxidation generates globin-derived peptides in atherosclerotic lesions and intraventricular hemorrhage of the brain, provoking endothelial dysfunction. Lab Invest 100:986-1002 (2020). PubMed: 32054994
- Nyakundi BB et al. Oxidized hemoglobin forms contribute to NLRP3 inflammasome-driven IL-1ß production upon intravascular hemolysis. Biochim Biophys Acta Mol Basis Dis 1865:464-475 (2019). PubMed: 30389578
- Potor L et al. Hydrogen Sulfide Abrogates Hemoglobin-Lipid Interaction in Atherosclerotic Lesion. Oxid Med Cell Longev 2018:3812568 (2018). PubMed: 29560080
- Gáll T et al. Heme Induces Endoplasmic Reticulum Stress (HIER Stress) in Human Aortic Smooth Muscle Cells. Front Physiol 9:1595 (2018). PubMed: 30515102