نتایج جستجو برای: genetic modifiers

تعداد نتایج: 620378  

Journal: :Haematologica 2016
Friederike Pastore Ross L Levine

Genomic studies of hematologic malignancies have identified a spectrum of recurrent somatic alterations that contribute to acute myeloid leukemia initiation and maintenance, and which confer sensitivities to molecularly targeted therapies. The majority of these genetic events are small, site-specific alterations in DNA sequence. In more than two thirds of patients with de novo acute myeloid leu...

2014
Wayne N. Frankel Connie L. Mahaffey Tracy C. McGarr Barbara J. Beyer Verity A. Letts

Absence epilepsy (AE) is a common type of genetic generalized epilepsy (GGE), particularly in children. AE and GGE are complex genetic diseases with few causal variants identified to date. Gria4 deficient mice provide a model of AE, one for which the common laboratory inbred strain C3H/HeJ (HeJ) harbors a natural IAP retrotransposon insertion in Gria4 that reduces its expression 8-fold. Between...

2017
Mattia Quattrocelli Joanna Capote Joyce C Ohiri James L Warner Andy H Vo Judy U Earley Michele Hadhazy Alexis R Demonbreun Melissa J Spencer Elizabeth M McNally

Genetic disruption of the dystrophin complex produces muscular dystrophy characterized by a fragile muscle plasma membrane leading to excessive muscle degeneration. Two genetic modifiers of Duchenne Muscular Dystrophy implicate the transforming growth factor β (TGFβ) pathway, osteopontin encoded by the SPP1 gene and latent TGFβ binding protein 4 (LTBP4). We now evaluated the functional effect o...

2009
A Driss KO Asare JM Hibbert BE Gee TV Adamkiewicz JK Stiles

More than half a century after the discovery of the molecular basis of Sickle Cell Disease (SCD), the causes of the phenotypic heterogeneity of the disease remain unclear. This heterogeneity manifests with different clinical outcomes such as stroke, vaso-occlusive episodes, acute chest syndrome, avascular necrosis, leg ulcers, priapism and retinopathy. These outcomes cannot be explained by the ...

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