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It is the note that I have skimmed from three different papers. 1. ZNRF3/RNF43--A direct linkage of extracellular recognition and E3 ligase activity to modulate cell surface signaling (doi:10.1016/j.pbiomolbio.2015.04.006) -- 2015 2. The structural basis of R-spondin recognition by LGR5 and RNF43 (doi:10.1101/gad.219915.113) -- 2013 3.The Role of the Transmembrane RING Finger Proteins in Cellular and Organelle Function (doi:10.3390/membranes1040354) -- 2011 RNF43 controls the abundance of Fz on the cell membrane. RNF43 is E3 ubiquitin ligase which adds Ub to the target molecule. RNF43 have three different domain; PA (ectodomain)-TM-RING (internal domain) Common feature of TM-E3 ligase -- self-ubiquitination, therefore, it remains low ubiquitination of targeted protein, like for RNF43 is Fz, for example --> interfering of self-ubiquitination --> afftect the abundance of E3-ligase's targeted protein.  RNF43 is paralogous to ZNRF3 but structural analysis, Z

Paper: RNF43 is frequently mutated in colorectal and endometrial cancers (doi: 10.1038/ng.3127) Before that there were the studies showed that RNF43 was the oncogene in colorectal cancer which meant that cancer cell overexpress this gene in order to keep the cancerous characteristic. Ten years later, this study showed that RNF43 was the tumor suppressor gene in MSI-colorectal cancer. The new discovery relies on the new technology as well as the way to categorize the cancer subtype, at the very beginning it depended on the cellular histology under the microscope, and lately, it has been shifted to the molecular level which can inform more detail on the pathogenesis, disease progression and the treatment outcomes. Note on this paper; colorectal cancer and endometrial cancer -- Wnt-dependent tumor type; MSI-common 1. whole exome sequencing of colorectal cancer (FFPE; 185 samples) 2. found out large number of RNF43 non-silent mutations; 18.9% of case 3. found frameshift mutatio