Andrew Beenken
New York University
24 Papers
30 Citations
Andrew Beenken is an academic researcher from New York University. The author has contributed to research in topics: Fibroblast growth factor & Biology. The author has an hindex of 12, co-authored 17 publications.
Chat about Author
Papers
The FGF family: biology, pathophysiology and therapy.
Andrew Beenken,Moosa Mohammadi +1 more
TL;DR: Traditional applications of recombinant FGFs and small-molecule FGF receptor kinase inhibitors in the treatment of cancer and cardiovascular disease and their emerging potential in thetreatment of metabolic syndrome and hypophosphataemic diseases are discussed.
Molecular insights into the klotho-dependent, endocrine mode of action of fibroblast growth factor 19 subfamily members
Regina Goetz,Andrew Beenken,Omar A. Ibrahimi,Juliya Kalinina,Shaun K. Olsen,Anna V. Eliseenkova,Chong Feng Xu,Thomas A. Neubert,Fuming Zhang,Fuming Zhang,Robert J. Linhardt,Xijie Yu,Kenneth E. White,Takeshi Inagaki,Steven A. Kliewer,Masaya Yamamoto,Hiroshi Kurosu,Yasushi Ogawa,Makoto Kuro-o,Beate Lanske,Mohammed S. Razzaque,Moosa Mohammadi +21 more
TL;DR: The crystal structures of FGF19 alone and FGF23 in complex with sucrose octasulfate, a disaccharide chemically related to heparin, are presented, showing that Klotho/βKlotho have evolved as a compensatory mechanism for the poor ability ofHeparin/heparan sulfate to promote binding of F GF19, -21, and -23 to their cognate receptors.
590
Decreased FGF8 signaling causes deficiency of gonadotropin-releasing hormone in humans and mice
John L. Falardeau,Wilson C. J. Chung,Andrew Beenken,Taneli Raivio,Lacey Plummer,Yisrael Sidis,Elka Jacobson-Dickman,Anna V. Eliseenkova,Jinghong Ma,Andrew A. Dwyer,Richard Quinton,Sandra Na,Janet E. Hall,Céline Huot,Natalie Alois,Simon H. S. Pearce,Lindsay W. Cole,Virginia A. Hughes,Moosa Mohammadi,Pei Tsai,Nelly Pitteloud +20 more
TL;DR: FGF8 is identified as a gene implicated in GnRH deficiency in both humans and mice and demonstrated an exquisite sensitivity of GnRH neuron development to reductions in FGF8 signaling.
Mutations in FGF17, IL17RD, DUSP6, SPRY4, and FLRT3 Are Identified in Individuals with Congenital Hypogonadotropic Hypogonadism
Hichem Miraoui,Andrew A. Dwyer,Andrew A. Dwyer,Gerasimos P. Sykiotis,Gerasimos P. Sykiotis,Lacey Plummer,Wilson C. J. Chung,Bihua Feng,Andrew Beenken,Jeffrey A Clarke,Tune H. Pers,Tune H. Pers,Tune H. Pers,Piotr Dworzynski,Kimberley Keefe,Marek Niedziela,Taneli Raivio,William F. Crowley,Stephanie B. Seminara,Richard Quinton,Virginia A. Hughes,Virginia A. Hughes,Philip Kumanov,Jacques Young,Maria A Yialamas,Janet E. Hall,Guy Van Vliet,Jean-Pierre Chanoine,John L.R. Rubenstein,Moosa Mohammadi,Pei-San Tsai,Yisrael Sidis,Yisrael Sidis,Kasper Lage,Nelly Pitteloud,Nelly Pitteloud +35 more
TL;DR: It is hypothesized that mutations in genes encoding a broader range of modulators of the FGFR1 pathway might contribute to the genetics of CHH as causal or modifier mutations and validate the ability of a bioinformatics algorithm on the basis of protein-protein interactome data (interactome-based affiliation scoring [IBAS]) to identify high-quality candidate genes.
Differential Interactions of FGFs with Heparan Sulfate Control Gradient Formation and Branching Morphogenesis
Helen P. Makarenkova,Helen P. Makarenkova,Matthew P. Hoffman,Andrew Beenken,Anna V. Eliseenkova,Robyn Meech,Robyn Meech,Cindy Tsau,Vaishali N. Patel,Richard A. Lang,Moosa Mohammadi +10 more
TL;DR: Differences in the binding of fibroblast growth factor 7 (FGF7) and FGF10 to heparan sulfate (HS) underlie the formation of different gradients that dictate distinct activities during branching morphogenesis, which may provide a general model for understanding how binding to HS regulates other morphogenetic gradients.