SCUBA

LRP4 — LDL receptor related protein 4

LRP4 belongs to a gene co-expression module in 1 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

LRP4's module in each cell type

Cell typeModuleShares the module with
FibroblastsWNT-modulating Fibroblast
Developmental
CIB2, COL4A5, DMKN, F3, FIP1L1, FRZB, GPSM3, HSD17B2 +9 moreView in SCUBA

About the gene

SynonymsCLSS, LRP-4, MEGF7, SOST2
Chromosome11: 46856717-46918642
Predicted locationIntracellular, Membrane
Essential geneNo
Protein classDisease related genes, Human disease related genes, Potential drug targets, Predicted intracellular proteins, Predicted membrane proteins, Transporters
Molecular functionDevelopmental protein, Receptor
Biological processDifferentiation, Endocytosis, Wnt signaling pathway

Function

Mediates SOST-dependent inhibition of bone formation. Functions as a specific facilitator of SOST-mediated inhibition of Wnt signaling. Plays a key role in the formation and the maintenance of the neuromuscular junction (NMJ), the synapse between motor neuron and skeletal muscle. Directly binds AGRIN and recruits it to the MUSK signaling complex. Mediates the AGRIN-induced phosphorylation of MUSK, the kinase of the complex. The activation of MUSK in myotubes induces the formation of NMJ by regulating different processes including the transcription of specific genes and the clustering of AChR in the postsynaptic membrane. Alternatively, may be involved in the negative regulation of the canonical Wnt signaling pathway, being able to antagonize the LRP6-mediated activation of this pathway. More generally, has been proposed to function as a cell surface endocytic receptor binding and internalizing extracellular ligands for degradation by lysosomes. May play an essential role in the process of digit differentiation (By similarity).

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.