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Fig. 1 | Cell Communication and Signaling

Fig. 1

From: Targeting the hedgehog pathway in MET mutation cancers and its effects on cells associated with cancer development

Fig. 1

The HGF/c-Met axis activates the Hh pathway through downstream signaling, including MAPK, PI3K/AKT, and STAT3, among others. HGF's kringle domains (K1-K4) structures activate c-Met, while the serine proteinase homology domain (SPH) and N-terminal (N) domains enhance receptor binding. The extracellular portion of c-Met consists of the SEMA domain, the plexin-semaphoring-integrin (PSI) domain, and four immunoglobulin-like regions in plexins and transcription factors (IPT1-4) domain. The intracellular portion includes the juxtamembrane (JM) domain, tyrosine kinase (TK) domain, and C-terminal multifunctional docking site (MFDS). The phosphorylation of S985 and Y1003 in the JM domain leads to ubiquitination-mediated degradation of c-Met, whereas the autophosphorylation of Y1234 and Y1235 in the TK domain upregulates pathway activity by triggering the phosphorylation of Y1349 and Y1356 in the MFDS. The phosphorylation of MFDS primarily serves to recruit downstream proteins

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Cell Communication and Signaling

ISSN: 1478-811X