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Fig. 8 | Journal of Hematology & Oncology

Fig. 8

From: The D Domain of LRRC4 anchors ERK1/2 in the cytoplasm and competitively inhibits MEK/ERK activation in glioma cells

Fig. 8

Schematic diagram of LRRC4 as a tumor suppressor in glioblastoma. The MEK/ERK/MAPK pathway is one of the most frequently aberrantly activated signaling pathways, and LRRC4 is an important tumor suppressor and has decreased expression in glioblastoma. Ectopic expression of LRRC4 abrogates the MEK1/2-ERK1/2 interaction. LRRC4 competitively inhibits the binding of ERK1/2 with MEK1/2 and prevents the phosphorylation of ERK1/2 and nucleus translocation. This further suppresses the ERK-mediated activation of the downstream transcripts to inhibit cell proliferation and invasion. In glioblastoma, the decrease or loss of LRRC4 failed to block the ERK 1/2-MEK 1/2 interaction and prevents MEK1/2 activation of ERK1/2

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