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MyoD is important in both muscle development and maintenance of the differentiated phenotype of type IIb fibers.
Most prominently, PPARβ deficiency increased myostatin levels both locally and systemically, which can negatively impact on both muscle development and osteoblastic function (31 – 31).
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Subsequently, we have confirmed that the expression of Hedgehog target genes ptc1 and nkx2.2a are severely inhibited in the Dmrt2b morphants, and both slow muscle development and neural tube development are also disrupted by Hedgehog pathway impairment.
Two of the four known myogenic regulatory factors (MRFs: myog, myf6) are down-regulated in the EO, both genes are fundamental for muscle development and differentiation [ 27]; in particular, knock-down experiments on myf6 have shown the degradation of posterior somites in D. rerio [ 28], the region where the adult EO originates [ 17].
Caenorhabditis elegans sarcomeres have been studied extensively utilizing both forward and reverse genetic techniques to provide insight into muscle development and the mechanisms behind muscle contraction.
Genes that increased in both cells derived from young and old rats are related to muscle development and cell cycle.
Both of these proteins are muscle-specific proteins, ENO3 being involved in muscle development and regeneration (Ohara et al, 2006), whereas TNNT3 is involved in striated muscle contraction.
Fusion of myoblasts into multinucleated myofibers is crucial for skeletal muscle development and regeneration.
The lysine methyltransferase Ehmt2/G9a is dispensable for skeletal muscle development and regeneration.
These proteins have also been shown to be involved in heart and muscle development and function in zebrafish muscle development17.
Skeletal muscle development and growth is a highly regulated process controlled by interactions between muscle cells and their surrounding microenvironment.
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