Identification of acquired somatic mutations in the gene encoding chromatin-remodeling factor ATRX in the alpha-thalassemia myelodysplasia syndrome (ATMDS).

Gibbons, RJ; Pellagatti, A; Garrick, D; Wood, WG; Malik, N; Ayyub, H; Langford, C; Boultwood, J; Wainscoat, JS; Higgs, DR

Abstract:

Inherited mutations of specific genes have elucidated the normal roles of the proteins they encode by relating specific mutations to particular phenotypes. But many potentially informative mutations in such genes are lethal early in development. Consequently, inherited mutations may not reflect all the functional roles of such proteins. Acquired, somatic defects should reflect a wider spectrum of mutations because they are not prone to negative selection in development. It has been difficult ...

Expand abstract

Publication status:

Published

Actions

Email

Email this record

Send the bibliographic details of this record to your email address.

Your Email
Please enter the email address that the record information will be sent to.

-
Your message (optional)
Please add any additional information to be included within the email.
Cite

Cite this record

APA Style

Gibbons, R. J., Pellagatti, A., Garrick, D., Wood, W. G., Malik, N., Ayyub, H., Langford, C., Boultwood, J., Wainscoat, J. S., & Higgs, D. R. (2003). Identification of acquired somatic mutations in the gene encoding chromatin-remodeling factor ATRX in the alpha-thalassemia myelodysplasia syndrome (ATMDS). Nature Genetics, 34(4), 446–449.

MLA Style

Gibbons, R. J., et al. “Identification of Acquired Somatic Mutations in the Gene Encoding Chromatin-Remodeling Factor ATRX in the Alpha-Thalassemia Myelodysplasia Syndrome (ATMDS).” Nature Genetics, vol. 34, no. 4, 2003, pp. 446–49.

Chicago Style

Gibbons, RJ, A Pellagatti, D Garrick, WG Wood, N Malik, H Ayyub, C Langford, J Boultwood, JS Wainscoat, and DR Higgs. 2003. “Identification of Acquired Somatic Mutations in the Gene Encoding Chromatin-Remodeling Factor ATRX in the Alpha-Thalassemia Myelodysplasia Syndrome (ATMDS).” Nature Genetics 34 (4): 446–49.
Tweet
Print