Key features and details
- Goat polyclonal to Hemoglobin
- Reacts with: Human
- Isotype: IgG
- Research with confidence – consistent and reproducible results with every batch
- Long-term and scalable supply – powered by recombinant technology for fast production
- Success from the first experiment – confirmed specificity through extensive validation
- Ethical standards compliant – production is animal-free
Product nameAnti-Hemoglobin antibody
See all Hemoglobin primary antibodies
DescriptionGoat polyclonal to Hemoglobin
Species reactivityReacts with: Human
Full length protein corresponding to Human Hemoglobin. Sheep were immunized with purified human hemoglobin F of fetal red blood cell origin.
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Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
Storage bufferpH: 6.8
Preservative: 0.1% Sodium azide
Constituents: 1.21% Tris, 0.02% Sodium chloride
Concentration information loading...
Purification notesAntiserum was solid phase adsorbed against hemoglobin A to ensure specificity. The antiserum was fractionated and passed over DEAE to yield an IgG fraction.
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
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
ab19363 has not yet been referenced specifically in any publications.