ⓘ RNF216

                                     

ⓘ RNF216

E3 ubiquitin-protein ligase RNF216 is an enzyme that in humans is encoded by the RNF216 gene.

This gene encodes a cytoplasmic protein which specifically colocalizes and interacts with the serine / threonine protein kinase, receptor interaction protein RIP. The zinc finger domains of the encoded protein necessary for interaction with rip and for inhibition of TNF and ИЛ1-induced factor NF-Kappa B pathway activation. The encoded protein may also function as a ubiquitin-protein E3 ubiquitin ligase which accepts from the E2-ubiquitin-conjugating enzymes and transfers it to substrates. Several alternative spliced variants of the transcript have been described for this locus but the full-length nature of only some of them.

                                     
  • RNF216 intronic transcript 1 is a protein that in humans is encoded by the RNF216 - IT1 gene. Human PubMed Reference: National Center for Biotechnology
  • polymerase III subunit RCP9 REPIN1: replication initiator 1 RNF216 - IT1: encoding protein RNF216 intronic transcript 1 SCIN: scinderin SCRN1: secernin 1 SOSTDC1:
  • enrolling Illuminate 301, NCT03445533 TLR9 has been shown to interact with RNF216 Epidermal growth factor receptor EGFR is constitutively bound to TLR9
  • interact with: BIRC2, BIRC3, CA11, CASP8, CFLAR, CRADD, RIPK2, RIPK3, RNF 11, RNF216 SQSTM1, TNFRSF1A, TRADD, TRAF2, UBC. clAP1 IAPs LUBAC IGF - 1R FLIP MLKL
  • RAS - like, estrogen - regulated, growth inhibitor RNF 34: encoding enzyme E3 ubiquitin - protein ligase RNF 34 SARNP: SAP domain - containing ribonucleoprotein
  • Cerebellar ataxia. Gordon Holmes syndrome Autosomal recessive Rare 609948 RNF216 RNF216 7p22.1 Cerebellar ataxia. Gordon Holmes syndrome Autosomal recessive
  • PDLIM2, PIAS3, PIM1, PIN1, PKA, POU2F1, PPARG, PPP1R13L, PRKCZ, REL, RFC1, RNF 25, SIRT1, SOCS1, SP1, STAT3, TAF4B, TBP, TP53, and TRIB3. Gene knockout of
  • genes: PCDH10, DIA1 formerly known as C3ORF58 NHE9, CNTN3, SCN7A, and RNF 8. Several of these genes appeared to be targets of MEF2, one of the transcription