ID:PLXB1_HUMAN DESCRIPTION: RecName: Full=Plexin-B1; AltName: Full=Semaphorin receptor SEP; Flags: Precursor; FUNCTION: Receptor for SEMA4D. Plays a role in RHOA activation and subsequent changes of the actin cytoskeleton. Plays a role in axon guidance, invasive growth and cell migration. SUBUNIT: Monomer, and heterodimer with PLXNB2 after proteolytic processing. Binds RAC1 that has been activated by GTP binding. Interaction with SEMA4D promotes binding of cytoplasmic ligands. Binds PLXNA1 (By similarity). Interacts with ARHGEF11, ARHGEF12, ERBB2, MET, MST1R, RRAS, RHOD, RND1, NRP1 and NRP2. INTERACTION: P08581:MET; NbExp=7; IntAct=EBI-1111488, EBI-1039152; Q04912:MST1R; NbExp=3; IntAct=EBI-1111488, EBI-2637518; SUBCELLULAR LOCATION: Isoform 1: Cell membrane; Single-pass type I membrane protein. SUBCELLULAR LOCATION: Isoform 2: Secreted. SUBCELLULAR LOCATION: Isoform 3: Secreted. TISSUE SPECIFICITY: Highly expressed in fetal kidney, and at slightly lower levels in fetal brain, lung and liver. PTM: Phosphorylated on tyrosine residues by ERBB2 and MET upon SEMA4D binding. PTM: Proteolytic processing favors heterodimerization with PLXNB2 and SEMA4D binding. SIMILARITY: Belongs to the plexin family. SIMILARITY: Contains 3 IPT/TIG domains. SIMILARITY: Contains 1 Sema domain. SEQUENCE CAUTION: Sequence=BAA23703.2; Type=Erroneous initiation; Note=Translation N-terminally shortened;
The RNAfold program from the Vienna RNA Package is used to perform the secondary structure predictions and folding calculations. The estimated folding energy is in kcal/mol. The more negative the energy, the more secondary structure the RNA is likely to have.
ModBase Predicted Comparative 3D Structure on O43157
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Orthologous Genes in Other Species
Orthologies between human, mouse, and rat are computed by taking the best BLASTP hit, and filtering out non-syntenic hits. For more distant species reciprocal-best BLASTP hits are used. Note that the absence of an ortholog in the table below may reflect incomplete annotations in the other species rather than a true absence of the orthologous gene.