Editing Hemoglobin (section)

==Types of hemoglobin in humans==
[[Hemoglobin variants]] are a part of the normal [[human embryonic development|embryonic]] and [[human fetal development|fetal]] development. They may also be pathologic mutant forms of hemoglobin in a [[population]], caused by variations in genetics. Some well-known hemoglobin variants, such as [[sickle-cell anemia]], are responsible for diseases and are considered [[hemoglobinopathy|hemoglobinopathies]]. Other variants cause no detectable [[pathology]], and are thus considered non-pathological variants.<ref name="Huisman-1996"/><ref>{{cite web |title=Hemoglobin Variants |date=2007-11-10 |website=Lab Tests Online |publisher=American Association for Clinical Chemistry |url=https://www.labtestsonline.org/understanding/analytes/hemoglobin_var/glance-3.html |access-date=2008-10-12 |url-status=live |archive-url=https://web.archive.org/web/20080920042335/https://www.labtestsonline.org/understanding/analytes/hemoglobin_var/glance-3.html |archive-date=2008-09-20}}</ref>

In [[embryo]]s:
* Gower 1 (ζ<sub>2</sub>ε<sub>2</sub>).
* Gower 2 (α<sub>2</sub>ε<sub>2</sub>) ({{PDB|1A9W}}).
* Hemoglobin Portland I (ζ<sub>2</sub>γ<sub>2</sub>).
* Hemoglobin Portland II (ζ<sub>2</sub>β<sub>2</sub>).

In fetuses:
* [[Hemoglobin F]] (α<sub>2</sub>γ<sub>2</sub>) ({{PDB|1FDH}}).

In [[neonate]]s (newborns inmmediately after birth):
* [[Hemoglobin A]] (adult hemoglobin) (α<sub>2</sub>β<sub>2</sub>) ({{PDB|1BZ0}}) – The most common with a normal amount over 95%
* [[Hemoglobin A2|Hemoglobin A<sub>2</sub>]] (α<sub>2</sub>δ<sub>2</sub>) – δ chain synthesis begins late in the third trimester and, in adults, it has a normal range of 1.5–3.5%
* [[Hemoglobin F]] (fetal hemoglobin) (α<sub>2</sub>γ<sub>2</sub>) – In adults Hemoglobin F is restricted to a limited population of red cells called F-cells. However, the level of Hb F can be elevated in persons with sickle-cell disease and [[beta-thalassemia]].
[[File:Postnatal genetics en.svg|thumb|upright=1.35|Gene expression of hemoglobin before and after birth. Also identifies the types of cells and organs in which the gene expression (data on ''Wood W.G.'', (1976). '''Br. Med. Bull. 32, 282.''')]]

Abnormal forms that occur in diseases:
* [[Hemoglobin D]] – (α<sub>2</sub>β<sup>D</sup><sub>2</sub>) – A variant form of hemoglobin.
* Hemoglobin H (β<sub>4</sub>) – A variant form of hemoglobin, formed by a tetramer of β chains, which may be present in variants of [[alpha-thalassemia|α thalassemia]].
* [[Hemoglobin Barts]] (γ<sub>4</sub>) – A variant form of hemoglobin, formed by a tetramer of γ chains, which may be present in variants of α thalassemia.
* [[Hemoglobin S]] (α<sub>2</sub>β<sup>S</sup><sub>2</sub>) – A variant form of hemoglobin found in people with sickle cell disease. There is a variation in the β-chain gene, causing a change in the properties of hemoglobin, which results in sickling of red blood cells.
* [[Hemoglobin C]] (α<sub>2</sub>β<sup>C</sup><sub>2</sub>) – Another variant due to a variation in the β-chain gene. This variant causes a mild chronic [[hemolytic anemia]].
* [[Hemoglobin E]] (α<sub>2</sub>β<sup>E</sup><sub>2</sub>) – Another variant due to a variation in the β-chain gene. This variant causes a mild chronic hemolytic anemia.
* Hemoglobin AS – A heterozygous form causing [[sickle cell trait]] with one adult gene and one sickle cell disease gene
* Hemoglobin SC disease – A compound heterozygous form with one sickle gene and another encoding [[hemoglobin C]].
* [[Hemoglobin Hopkins-2]] – A variant form of hemoglobin that is sometimes viewed in combination with [[hemoglobin S]] to produce sickle cell disease.