Institution
Regeneron
Company•Tarrytown, New York, United States•
About: Regeneron is a company organization based out in Tarrytown, New York, United States. It is known for research contribution in the topics: Dupilumab & Population. The organization has 2368 authors who have published 2985 publications receiving 218416 citations.
Papers published on a yearly basis
Papers
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TL;DR: New findings in newly discovered vascular growth factors demand re-evaluation of therapeutic efforts aimed at regulating blood vessel growth in ischaemia, cancer and other pathological settings.
Abstract: A recent explosion in newly discovered vascular growth factors has coincided with exploitation of powerful new genetic approaches for studying vascular development. An emerging rule is that all of these factors must be used in perfect harmony to form functional vessels. These new findings also demand re-evaluation of therapeutic efforts aimed at regulating blood vessel growth in ischaemia, cancer and other pathological settings.
3,726 citations
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TL;DR: Two genes encode ubiquitin ligases that are potential drug targets for the treatment of muscle atrophy, and mice deficient in either MAFbx orMuRF1 were found to be resistant to atrophy.
Abstract: Skeletal muscle adapts to decreases in activity and load by undergoing atrophy. To identify candidate molecular mediators of muscle atrophy, we performed transcript profiling. Although many genes were up-regulated in a single rat model of atrophy, only a small subset was universal in all atrophy models. Two of these genes encode ubiquitin ligases: Muscle RING Finger 1 (MuRF1), and a gene we designate Muscle Atrophy F-box (MAFbx), the latter being a member of the SCF family of E3 ubiquitin ligases. Overexpression of MAFbx in myotubes produced atrophy, whereas mice deficient in either MAFbx or MuRF1 were found to be resistant to atrophy. These proteins are potential drug targets for the treatment of muscle atrophy.
3,174 citations
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TL;DR: It is shown that mice engineered to lack Angiopoietin-1 display angiogenic deficits reminiscent of those previously seen in mice lacking TIE2, demonstrating that AngiopOietIn-1 is a primary physiologic ligand for TIE1 and that it has critical in vivo angiogenesis actions that are distinct from VEGF and that are not reflected in the classic in vitro assays used to characterize VEGf.
2,895 citations
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TL;DR: A revised version of the ALSFRS, which incorporates additional assessments of dyspnea, orthopnea, and the need for ventilatory support is validated, indicating that the quality of function is a strong determinant of quality of life in ALS.
2,440 citations
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TL;DR: It is concluded that the activation of the Akt/mTOR pathway and its downstream targets, p70S6K and PHAS-1/4E-BP1, is requisitely involved in regulating skeletal muscle fibre size, and that activation of this pathway can oppose muscle atrophy induced by disuse.
Abstract: Skeletal muscles adapt to changes in their workload by regulating fibre size by unknown mechanisms. The roles of two signalling pathways implicated in muscle hypertrophy on the basis of findings in vitro, Akt/mTOR (mammalian target of rapamycin) and calcineurin/NFAT (nuclear factor of activated T cells), were investigated in several models of skeletal muscle hypertrophy and atrophy in vivo. The Akt/mTOR pathway was upregulated during hypertrophy and downregulated during muscle atrophy. Furthermore, rapamycin, a selective blocker of mTOR, blocked hypertrophy in all models tested, without causing atrophy in control muscles. In contrast, the calcineurin pathway was not activated during hypertrophy in vivo, and inhibitors of calcineurin, cyclosporin A and FK506 did not blunt hypertrophy. Finally, genetic activation of the Akt/mTOR pathway was sufficient to cause hypertrophy and prevent atrophy in vivo, whereas genetic blockade of this pathway blocked hypertrophy in vivo. We conclude that the activation of the Akt/mTOR pathway and its downstream targets, p70S6K and PHAS-1/4E-BP1, is requisitely involved in regulating skeletal muscle fibre size, and that activation of the Akt/mTOR pathway can oppose muscle atrophy induced by disuse.
2,439 citations
Authors
Showing all 2386 results
Name | H-index | Papers | Citations |
---|---|---|---|
Richard A. Flavell | 231 | 1328 | 205119 |
Gonçalo R. Abecasis | 179 | 595 | 230323 |
George D. Yancopoulos | 158 | 496 | 93955 |
Masashi Yanagisawa | 130 | 524 | 83631 |
James E. Darnell | 123 | 287 | 67038 |
Alan R. Shuldiner | 120 | 557 | 71737 |
Henry N. Ginsberg | 104 | 413 | 51009 |
Jorge E. Galán | 102 | 221 | 34982 |
Melanie H. Cobb | 99 | 294 | 41086 |
Wayne A. Hendrickson | 94 | 313 | 38618 |
Friedrich Lottspeich | 94 | 449 | 30250 |
Sharon L.R. Kardia | 90 | 454 | 34842 |
John L. Rinn | 89 | 200 | 71982 |
Michael Sendtner | 88 | 269 | 31409 |
Jeffrey G. Reid | 88 | 227 | 86131 |