Gerard Grosveld
St. Jude Children's Research Hospital
158 Papers
4.3K Citations
Gerard Grosveld is an academic researcher from St. Jude Children's Research Hospital. The author has contributed to research in topics: Chromosomal translocation & Myeloid leukemia. The author has an hindex of 63, co-authored 155 publications. Previous affiliations of Gerard Grosveld include University of Tennessee Health Science Center & The Catholic University of America.
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Papers
Lack of Prox1 Downregulation Disrupts the Expansion and Maturation of Postnatal Murine β-Cells
Leena Paul,Emily M. Walker,Yiannis Drosos,Holly A. Cyphert,Geoffrey Neale,Roland Stein,Jack South,Gerard Grosveld,Pedro Luis Herrera,Beatriz Sosa-Pineda,Beatriz Sosa-Pineda +10 more
TL;DR: It is determined that Prox1 upregulation reduces proliferation, impairs maturation, and enables apoptosis in postnatal β-cells, and reducing the expression of ProX1 is beneficial for the expansion and maturation of postnatalβ-cells.
c-sis is translocated from chromosome 22 to chromosome 9 in chronic myelocytic leukemia
John Groffen,Nora Heisterkamp,John R. Stephenson,A G van Kessel,A. de Klein,Gerard Grosveld,Dirk Bootsma +6 more
TL;DR: The human oncogene, c-sis, is localized on the q11 to qter segment of chromosome 22 and its translocation from chromosome 22 to chromosome 9 (q34) in CML is demonstrated.
The human homologue of yeast CRM1 is in a dynamic subcomplex with CAN/Nup214 and a novel nuclear pore component Nup88.
Maarten Fornerod,Jan M. van Deursen,Sjozef van Baal,Albert B. Reynolds,Donna S. Davis,K. Gopal Murti,Jack Fransen,Gerard Grosveld +7 more
TL;DR: The oncogenic nucleoporin CAN/Nup214 is essential in vertebrate cells and it is proposed that hCRM1 is a soluble nuclear transport factor that interacts with the NPC, which is a novel nuclear pore complex (NPC) component named Nup88.
Overexpression of N-Myc rapidly causes acute myeloid leukemia in mice.
TL;DR: The results show that N-Myc overexpression is highly oncogenic in mouse myeloid cells and suggest thatN-MYC up-regulation contributes to human myeloids leukemogenesis.
Tel induces a G1 arrest and suppresses Ras-induced transformation
TL;DR: It is found that overexpression of Tel retards proliferation of many cell types, primary cells and immortalized cells, by inducing a G1 arrest, and Tel's block of cellular proliferation is rescued by high seeding densities.