Mean corpuscular hemoglobin is not increased in Fmr1 knockout mice

A slight increase in mean corpuscular hemoglobin (MCH) has been reported in erythrocytes from human fragile X patients. As it is difficult to perform case-controlled studies in patients with fragile X syndrome, we studied MCH in erythrocytes from transgenic mice with an Fmr1 knockout. None of the kn...

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Veröffentlicht in:	Human genetics 1996, Vol.97 (1), p.49-50
Hauptverfasser:	REYNIERS, E, VAN BOCKSTAELE, D. R, DE BOULLE, K, KOOY, R. F, BAKKER, C. E, OOSTRA, B. A, WILLEMS, P. J
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Biological and medical sciences Chromosome fragility (bloom syndrome, ataxia telangiectasia, fanconi anemia, x-linked mental retardation...) Erythrocytes - metabolism Fragile X Mental Retardation Protein Fragile X Syndrome - blood Fragile X Syndrome - genetics Hemoglobins - metabolism Humans Male Medical genetics Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Nerve Tissue Proteins - deficiency Nerve Tissue Proteins - genetics Reference Values RNA-Binding Proteins - genetics
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Zusammenfassung:	A slight increase in mean corpuscular hemoglobin (MCH) has been reported in erythrocytes from human fragile X patients. As it is difficult to perform case-controlled studies in patients with fragile X syndrome, we studied MCH in erythrocytes from transgenic mice with an Fmr1 knockout. None of the knockout mice showed increased MCH levels when compared with normal littermates. We conclude that it is unlikely that the FMR1 gene product has an effect on MCH.
ISSN:	0340-6717 1432-1203
DOI:	10.1007/BF00218832