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1 e wasting in an inflammatory myopathy model (cardiotoxin).
2 es before and after muscle injury induced by cardiotoxin.
3 n was induced by injuring mouse muscles with cardiotoxin.
4 d dramatically from 1 to 3 d after injury by cardiotoxin.
5 doxorubicin-induced cardiotoxicity and other cardiotoxins.
6 generation, we injured wild-type muscle with cardiotoxin and found that Akt induced a faster regenera
7 protected muscle from both acute injury with cardiotoxin and from chronic muscle disease in the mdx o
9 ted in PDGFRbeta(+) cells are protected from cardiotoxin and laceration-induced skeletal muscle fibro
14 kinetics of over 100 proteins in response to cardiotoxin (CTX) induced muscle damage and regeneration
19 bustly in regenerating skeletal muscle after cardiotoxin (CTX)-induced muscle injury in vivo and diff
20 ythroid-derived-2)-like 2 (Nrf2), aggravates cardiotoxin (CTX)-induced tibialis anterior (TA) muscle
26 the discovery of a new insulinotropic agent, cardiotoxin-I (CTX-I), from the Naja kaouthia snake veno
28 MyoR and miR-378 were anticorrelated during cardiotoxin-induced adult muscle regeneration in mice.
30 ed cells and macrophages were assessed after cardiotoxin-induced injury of chimeric mice produced by
31 c conditions, regeneration was delayed after cardiotoxin-induced injury, with prolonged necrosis most
37 dels, we studied regeneration consecutive to cardiotoxin-induced muscle injury and observed a signifi
39 ers (MyoD, myogenin, and active-Notch) after cardiotoxin-induced muscle injury in vivo and in SCs cul
41 smaller size of newly formed myofibers after cardiotoxin-induced muscle injury, increased glycolysis,
45 licited by immunization with pVCL/MSP1a into cardiotoxin-induced regenerating muscle were evaluated i
46 ntiation and prolonged Pax7 expression after cardiotoxin-induced skeletal muscle injury, while single
47 ments revealed that Staufen1 increases after cardiotoxin injection before returning to the low levels
51 ersion of marrow cells to skeletal muscle in cardiotoxin-injured anterior tibialis muscle in a green
52 c gene expression and muscle regeneration in cardiotoxin-injured beta3-integrin-null mice are impaire
53 neration and that gene transfer of GEFT into cardiotoxin-injured mouse tibialis anterior muscle exert
54 ed that SP cells isolated from dystrophic or cardiotoxin-injured muscle fail to undergo myogenesis.
57 ransplantation of these committed cells into cardiotoxin-injured skeletal muscles of NOD/SCID mice re
58 d damage, exhibit delayed regeneration after cardiotoxin injury and suffer from defective myoblast fu
62 njury and improved muscle regeneration after cardiotoxin injury, as well as increased satellite cell
63 vivo model of muscle regeneration following cardiotoxin injury, ectopic miR-431 injection greatly im
73 und delay in satellite cell activation after cardiotoxin treatment in alpha7 integrin-null animals wh
74 beta1 integrin plays in muscle regeneration, cardiotoxin was used to induce damage in the tibialis an