Key features and details
- FITC Goat polyclonal to Hemoglobin
- Reacts with: Human
- Conjugation: FITC. Ex: 493nm, Em: 528nm
- Isotype: IgG
Product nameFITC Anti-Hemoglobin antibody
See all Hemoglobin primary antibodies
DescriptionFITC Goat polyclonal to Hemoglobin
ConjugationFITC. Ex: 493nm, Em: 528nm
Species reactivityReacts with: Human
Predicted to work with: Chimpanzee, Rhesus monkey, Gorilla
F/P ratio is 3 to 7.
Reproducibility is key to advancing scientific discovery and accelerating scientists’ next breakthrough.
Abcam is leading the way with our range of recombinant antibodies, knockout-validated antibodies and knockout cell lines, all of which support improved reproducibility.
We are also planning to innovate the way in which we present recommended applications and species on our product datasheets, so that only applications & species that have been tested in our own labs, our suppliers or by selected trusted collaborators are covered by our Abpromise™ guarantee.
In preparation for this, we have started to update the applications & species that this product is Abpromise guaranteed for.
We are also updating the applications & species that this product has been “predicted to work with,” however this information is not covered by our Abpromise guarantee.
Applications & species from publications and Abreviews that have not been tested in our own labs or in those of our suppliers are not covered by the Abpromise guarantee.
Please check that this product meets your needs before purchasing. If you have any questions, special requirements or concerns, please send us an inquiry and/or contact our Support team ahead of purchase. Recommended alternatives for this product can be found below, as well as customer reviews and Q&As.
Storage instructionsShipped at 4°C. Store at +4°C.
Storage bufferpH: 6.8
Preservative: 0.1% Sodium azide
Constituents: PBS, 0.2% BSA
Concentration information loading...
PurityImmunogen affinity purified
Purification notesThe antibody was isolated by affinity chromatography using antigen coupled to agarose beads. Antibody concentration was determined by extinction coefficient prior to conjugation: absorbance at 280 nm of 1.4 equals 1.0 mg of IgG.
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
ab19361 has not yet been referenced specifically in any publications.