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Gas6‐Axl Double Knockout in Mice Decreases Skeletal Muscle mass Despite Elevated Anabolic Intracellular Signaling
Author(s) -
Olsen Zachary E.,
Mervis Matthew J.,
Matsumura Marc S.,
Hirschi-Budge Kelsey M.,
Arroyo Juan A.,
Reynolds Paul R.,
Thomson David
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.09757
Subject(s) - anabolism , gas6 , protein kinase b , p70 s6 kinase 1 , endocrinology , medicine , mapk/erk pathway , skeletal muscle , receptor tyrosine kinase , signal transduction , biology , kinase , chemistry , microbiology and biotechnology
Growth arrest specific‐6 (Gas6) is a signaling factor that has been shown to contribute to growth and survival in various cell types. It functions primarily by activating the receptor tyrosine kinase Axl. Very little is known about the role of Gas6‐Axl in skeletal muscle. Therefore, we studied muscle size and anabolic signaling in Gas6‐Axl double knock‐out mice (dKO). Hindlimb muscle mass was decreased in dKO mice. Skeletal muscle phosphorylation of Akt was not affected by genotype. However, extracellular signal‐related kinase (Erk), ribosomal protein subunit 6 (S6) and p70S6 kinase (S6k) phosphorylation was elevated in dKO muscles. We conclude, therefore, that anabolic signaling through these pathways does not explain the difference in muscle mass between genotypes. We speculate that the elevated anabolic signaling in dKO muscles is perhaps an adaptive compensation for other impaired anabolic processes in these muscles. Support or Funding Information This work was supported by a grant from the Flight Attendant’s Medical Research Institute (FAMRI) and a BYU Graduate Research Fellowship.