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Institution

Fred Hutchinson Cancer Research Center

NonprofitCape Town, South Africa
About: Fred Hutchinson Cancer Research Center is a nonprofit organization based out in Cape Town, South Africa. It is known for research contribution in the topics: Population & Transplantation. The organization has 12322 authors who have published 30954 publications receiving 2288772 citations. The organization is also known as: Fred Hutch & The Hutch.


Papers
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Journal ArticleDOI
28 Sep 1989-Nature
TL;DR: The pattern of expression of MyoDl and myogenin during the early stages of muscle formation in the mouse embryo in vivo and in limb-bud explants cultured in vitro indicates that they may have different functions in different types of muscle during development.
Abstract: MyoDl and myogenin are muscle-specific proteins which can convert non-myogenic cells in culture to differentiated muscle fibres, implicating them in myogenic determination The pattern of expression of MyoDl and myogenin during the early stages of muscle formation in the mouse embryo in vivo and in limb-bud explants cultured in vitro, indicates that they may have different functions in different types of muscle during development

640 citations

Journal ArticleDOI
28 Jun 1996-Cell
TL;DR: The death of Brca1(5-6) mutant embryos prior to gastrulation may be due to a failure of the proliferative burst required for the development of the different germ layers, and the fact that mutant blastocyst growth is grossly impaired in vitro.

640 citations

Journal ArticleDOI
16 Oct 1997-Nature
TL;DR: The similar phenotypes of reeler, scrambler, yotari and mdab1 null mice indicate that Reelin and mDab1 function as signalling molecules that regulate cell positioning in the developing brain.
Abstract: Formation of the mammalian brain requires choreographed migration of neurons to generate highly ordered laminar structures such as those in the cortices of the forebrain and the cerebellum. These processes are severely disrupted by mutations in reelin1 which cause widespread misplacement of neurons and associated ataxia in reeler mice2,3. Reelin is a large extracellular protein secreted by pioneer neurons that coordinates cell positioning during neurodevelopment1,4,5,6,7,8. Two new autosomal recessive mouse mutations, scrambler9 and yotari10 have been described that exhibit a phenotype identical to reeler9,10,11. Here we report that scrambler and yotari arise from mutations in mdab1 (ref. 12), a mouse gene related to the Drosophila gene disabled ( dab )13. Both scrambler and yotari mice express mutated forms of mdab1 messenger RNA and little or no mDab1 protein. mDab1 is a phosphoprotein that appears to function as an intracellular adaptor in protein kinase pathways. Expression analysis indicates that mdab1 is expressed in neuronal populations exposed to Reelin. The similar phenotypes of reeler, scrambler, yotari and mdab1 null mice14 indicate that Reelin and mDab1 function as signalling molecules that regulate cell positioning in the developing brain.

639 citations

Journal ArticleDOI
TL;DR: It is shown that inhibiting Inr/PI3K signaling phenocopies the cellular and organismal effects of starvation, whereas activating this pathway bypasses the nutritional requirement for cell growth, causing starvation sensitivity at the organismal level.

637 citations

Journal ArticleDOI
17 Sep 1999-Cell
TL;DR: The results indicate that dMyc links patterning signals to cell division by regulating primary targets involved in cellular growth and metabolism.

637 citations


Authors

Showing all 12368 results

NameH-indexPapersCitations
Walter C. Willett3342399413322
Robert Langer2812324326306
Meir J. Stampfer2771414283776
JoAnn E. Manson2701819258509
David J. Hunter2131836207050
Peer Bork206697245427
Eric Boerwinkle1831321170971
Ruedi Aebersold182879141881
Bruce M. Psaty1811205138244
Aaron R. Folsom1811118134044
David Baker1731226109377
Frederick W. Alt17157795573
Lily Yeh Jan16246773655
Yuh Nung Jan16246074818
Charles N. Serhan15872884810
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20237
202275
20211,981
20201,995
20191,685
20181,571