M
Michael K. Gross
Researcher at Salk Institute for Biological Studies
Publications - 9
Citations - 2970
Michael K. Gross is an academic researcher from Salk Institute for Biological Studies. The author has contributed to research in topics: Cellular differentiation & Germline. The author has an hindex of 9, co-authored 9 publications receiving 2845 citations. Previous affiliations of Michael K. Gross include European Bioinformatics Institute.
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Journal ArticleDOI
Germline regulatory element of Oct-4 specific for the totipotent cycle of embryonal cells
Young Il Yeom,Guy Fuhrmann,Catherine E. Ovitt,Alexander Brehm,Kazuyuki Ohbo,Michael K. Gross,Karin Hübner,Hans R. Schöler +7 more
TL;DR: Oct-4 expression in the germline is regulated separately from epiblast expression, and this provides the first marker for the identification of totipotent cells in the embryo, and suggests that expression of Oct-4 in the Totipotent cycle is dependent on a set of factors unique to the germ line.
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Lbx1 Specifies Somatosensory Association Interneurons in the Dorsal Spinal Cord
TL;DR: In mice lacking Lbx1, cells types that arise in the ventral alar plate acquire more dorsal identities, which results in the loss of dorsal horn association interneurons, excess production of commissural neurons, and disrupted sensory afferent innervation of the dorsal horn.
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New POU dimer configuration mediates antagonistic control of an osteopontin preimplantation enhancer by Oct-4 and Sox-2.
Valérie Botquin,Heike Hess,Guy Fuhrmann,Constantinos Anastassiadis,Michael K. Gross,Gerrit Vriend,Hans R. Schöler +6 more
TL;DR: The POU transcription factor Oct-4 is expressed specifically in the germ line, pluripotent cells of the pregastrulation embryo and stem cell lines derived from the early embryo.
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Lbx1 is required for muscle precursor migration along a lateral pathway into the limb.
TL;DR: Results suggest that Lbx1 regulates responsiveness to a lateral migration signal which emanates from the developing limb, and is necessary for the lateral, but not ventral, migration of hypaxial muscle precursors.
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The winged-helix transcription factor Foxd3 suppresses interneuron differentiation and promotes neural crest cell fate
TL;DR: Foxd3 can function independently of Slug and RhoB to promote the development of neural crest cells from neural tube progenitors, suggesting that Foxd3 may regulate aspects of the neural crest differentiation program.