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The most prominent amplification of Shh response was seen when Sema3F was added to cells in the presence of a high concentration of Shh (2 μg/ml).
This is consistent with the predicted role of Gli3 as a repressor of the Shh response.
Activation of the BMP response is sufficient to maintain gli3 expression in neural plate explants, which might be a mechanism by which BMPs antagonize the Shh response.
Misexpression of Gli3R* in the chick neural tube caused a ventral expansion of class-I, dorsal progenitor proteins and a loss of class-II, ventral progenitor proteins consistent with expected activity as a repressor of the Shh response.
GLI3 and GLI2 can act both as transcriptional activators or repressors whereas GLI1, whose expression is transcriptionally regulated by GLI2 and GLI3, appears to play a secondary role in potentiating the SHH response [15] [18].
This Shh response controls the expression of important transcription factors, which in turn direct differentiation into specific neuronal subtypes.
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Thus, removal of Gas1 leads to blunted Shh-N response in proliferation and elevated Gdnf response in differentiation.
Both of these findings suggest that 20(S -OHC iS -OHCthe Ptch1-regulated lisanotthet modulates Smo activity in response to Shh reception.
Exogenous SHH: In response to exogenous SHH, Vegfa expression is increased distally in sub-mesothelial mesenchyme.
Such post-natal reactivation of the embryonic signaling pathways implying Shh in response to muscle injury in the animal models incurred enhanced angiomyogenic response [4], [5].
Based on in vitro and genetic studies, the zinc finger-containing transcription factors Gli 1, 2, and 3 are mediators of the Shh intracellular response.
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Justyna Jupowicz-Kozak
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