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Before I came to SRC I worked with a charity in Beirut and taught English in Palestinian refugee camps in Lebanon and Syria.
To investigate the role of FAK in this mechanism, we now analyzed the phosphorylation and activation status of Src (i.e., phosphorylation at Y416) in control and FAK-depleted cells, which showed that FAK deficiency rendered Src hypophosphorylated in 4T1 cells.
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Cells expressing GFP, YFP, or both fluorescent proteins were isolated and collected 48 hours later on a MoFlo cell sorter (Cytomation, Fort Collins, CO, USA), and subsequently were expanded to yield stable polyclonal populations of control (i.e. GFP or YFP), β3 integrin (i.e. WT or D119A), or mutant c-Src (i.e. kinase-dead or constitutively active) expressing cells.
(E ) In the PI3K/AKT subnetwork, the SRC nodes (i.e., phosphorylation, total level, activity) are upstream of PI3K and AKT (total level, AKTpS473 and AKTp308) and the AKT nodes are the major hubs.
In turn, GLP-1 promoted angiogenesis in a dose-dependent manner, which was decreased by Akt inhibitor IV, a PKC inhibitor and src inhibitor I in a 3D culture system where spherules of HUVEC were embedded in a collagen scaffold [ 13].
Antibodies against the phosphorylated forms of Akt pS473, Erk1/2 pT185/pY187 and c-Src pY418 (i.e. phospho-specific antibodies), and corresponding pan-Akt and pan-Erk1/2 antibodies were obtained from Medicorp (Montreal, Quebec, Canada).
Anti-LRP-1 α-chain (8G1), anti-LRP-1 β-chain (5A6), anti-human IgGs used as negative control for immunoprecipitation experiments (HP6030), specific SAPK/JNK inhibitor SP600125 (420119) and Src kinase inhibitor I (567805) were obtained from Calbiochem (distributed by VWR International, Strasbourg, France).
Since with the exception of pYEEI, no crystal structures are available for these complexes the starting models for this simulations were built from the crystal structure of the Src SH2-pYEEI complex (PDB code: 1SPS), in which the Ile pTyr+3) was replaced by Leu, Val, Ala and Gly, respectively.
Therefore, the average delay D ¯ ( n + 1 ) can be obtained as follows: Figure 13 Tree-based computation of the average delay D ¯ ( m ), when m = n + 1. D ¯ ( n + 1 ) = T src tx + ∑ i = 1 n D ¯ i | i p Y ( i | S ).
On the basis of the approach described in detail in Appendix 4, the average end-to-end delay can be given the following recursive formulation: D ≜ D ¯ ( N ) = T ¯ src tx + ∑ i = 1 n D ¯ ( N - i ) + D ¯ i | i p Y ( i | S ) (10).
We address the hypothesis that myelin-mediated inhibition of OPC differentiation is mediated by (i) Src-family (Fyn-1)–RhoA-ROCK-II signalling or (ii) protein kinase C (PKC) pathway signalling.
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