IndraLab

Statements

SRC increases the amount of EGFR. 14 / 20
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"Indeed, this treatment increases EGFR expression, induces Src activation and caveolae mediated EGFR endocytosis."
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"Rutin's inhibition of Src kinase reduces the phosphorylation levels of EGFR and ERK, which may mitigate podocyte injury."
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"Very recently, c-Src has been demonstrated to mediate EGFR proligand release by MMPs, such as TGFα in head and neck squamous cell carcinoma [41] or amphiregulin in human keratinocytes [42] ."
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"Src is a well-established oncogenic partner of EGFR and although the underlying mechanisms remain to be fully identified, active/oncogenic Src can increase the amount of EGFR at the cell surface and i[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Interestingly, EGFR protein levels also increased, which may be attributed to Src’s role as an upstream regulator upregulating EGFR, or it could result from active Src restoring EGFR expression through compensatory mechanisms."
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"Consistent with these findings, siRNA silencing of Src also effectively reduced in vitro invasion of EGFR expressing LN229 glioblastoma cells (XREF_FIG)."
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"The constitutively activated Src allele did not initially enhance growth of EGFRvIII expressing tumors, but eventually conferred a modest growth enhancement once the tumors had become very large (XREF_FIG, p = 0.03)."
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"Our results showed that overexpression of EGFR or activated Src partially reduced YC-1-mediated growth inhibition, indicating their potential involvement in the anti-proliferative mechanism of YC-1."
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"Knockdown of c-Src inhibited UVB-induced COX-2 expression and phosphorylation of MAPKs and EGFR in HaCaT cells."
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"To confirm our hypothesis, we conducted a DARTS assay and revealed that 4‐PP increased c‐Src stability against pronase treatment (Figure 4C).3.5 Knockdown of c-Src inhibits UVB-induced COX-2 expression and phosphorylation of MAPKs and EGFR in HaCaT cells."
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"Parsons et al. first showed c-Src overexpression in EGFR expressing metastatic breast and other cancer cells promoted cell migration XREF_BIBR."
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"Some studies indicate that c-Src can upregulate EGFR levels by inhibiting receptor ubiquitylation and endocytosis."
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"Of note, cancer driver genes are also involved in dysregulated EGFR trafficking, that mutant p53 can trigger internalized EGFR recycling by inducing the interaction with the Rab11 effector Rab-couplin[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"FHL1 interacts with the transcription factor SP1 to upregulate EGFR expression and activate the downstream signaling cascades, including Src, Akt, Erk1/2, and Stat3, leading to glioblastoma malignancy."
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