In canonical SMAD signaling, TGFβ ligands (e.g., myostatin) bind to cell surface receptors, which initiate receptor-mediated phosphorylation of SMAD2 on its C-terminus (pSMAD2-C), followed by SMAD2 translocation to the nucleus and transcriptional activation23,24.
Tiny Trojan horses deliver a cancer drug to cell nuclei.
Interestingly, TIMP-1 binds to cell surface targets and translocates into the nucleus.
PI penetrates the cell membrane of damaged cells and binds to the cell nucleus.
We also monitored GnRHR trafficking and found that anti-HA bound to cell surface GnRHR and then trafficked to bright points that were prevalent around the nucleus.
When hybridoma cells secreting B3 were implanted into mice with severe combined immunodeficiency (SCID), the antibody was shown to penetrate cells and bind to their nuclei, both in the kidney and in other organs [ 8].
In the genomic mechanism, T3 accesses to the cell nucleus to bind THR, which disengages corepressors in favor of coactivators to thyroid hormone responsive element.
These bind to SMAD4 and migrate to the cell nucleus where they act as transcription factors and participate in the transcription of particular genes.
Through the phosphorylation, IκBα dissociates from the complex and the p65 and p50 subunits freely translocate to the cell nucleus and bind to NF-κB recognition sites in the promoter regions of various NF-κB-regulated genes.
Once activated, STAT3 forms homodimers, translocate to the cell nucleus and binds to specific regulatory DNA elements to induce transcription.
