ROR1

ROR1
Identifiers
Aliases	ROR1, NTRKR1, dJ537F10.1, receptor tyrosine kinase-like orphan receptor 1, receptor tyrosine kinase like orphan receptor 1
External IDs	OMIM: 602336; MGI: 1347520; HomoloGene: 3675; GeneCards: ROR1; OMA:ROR1 - orthologs
Gene location (Human) Chr. Chromosome 1 (human)[1] Band 1p31.3 Start 63,774,017 bp[1] End 64,181,498 bp[1]
Gene location (Mouse) Chr. Chromosome 4 (mouse)[2] Band 4 C6|4 45.71 cM Start 99,952,988 bp[2] End 100,301,962 bp[2]
RNA expression pattern Bgee Human Mouse (ortholog) Top expressed in germinal epithelium popliteal artery tibial arteries islet of Langerhans right coronary artery lower lobe of lung saphenous vein Descending thoracic aorta sural nerve buccal mucosa cell Top expressed in epithelium of lens gastrula belly cord abdominal wall decidua medullary collecting duct atrioventricular valve efferent ductule vestibular sensory epithelium maxillary prominence More reference expression data BioGPS n/a
Gene ontology Molecular function transmembrane receptor protein tyrosine kinase activity nucleotide binding protein binding protein kinase activity Wnt-protein binding kinase activity ATP binding transferase activity coreceptor activity involved in Wnt signaling pathway, planar cell polarity pathway Wnt-activated receptor activity receptor tyrosine kinase transmembrane signaling receptor activity Cellular component receptor complex integral component of plasma membrane integral component of membrane membrane stress fiber cytoplasm cell surface plasma membrane axon terminus axon cell projection Biological process phosphorylation protein phosphorylation Wnt signaling pathway transmembrane receptor protein tyrosine kinase signaling pathway Wnt signaling pathway, planar cell polarity pathway peptidyl-tyrosine phosphorylation astrocyte development hearing positive regulation of I-kappaB kinase/NF-kappaB signaling inner ear development positive regulation of NF-kappaB transcription factor activity negative regulation of signal transduction cell differentiation negative regulation of apoptotic process positive regulation of ERK1 and ERK2 cascade anatomical structure development Sources:Amigo / QuickGO
Orthologs Species Human Mouse Entrez 4919 26563 Ensembl ENSG00000185483 ENSMUSG00000035305 UniProt Q01973 Q9Z139 RefSeq (mRNA) NM_001083592 NM_005012 NM_013845 NM_001312690 RefSeq (protein) NP_001077061 NP_005003 NP_001299619 NP_038873 Location (UCSC) Chr 1: 63.77 – 64.18 Mb Chr 4: 99.95 – 100.3 Mb PubMed search [3] [4]
Wikidata
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Tyrosine-protein kinase transmembrane receptor ROR1, also known as neurotrophic tyrosine kinase, receptor-related 1 (NTRKR1), is an enzyme that in humans is encoded by the ROR1 gene.^[5][6][7] ROR1 is a member of the receptor tyrosine kinase-like orphan receptor (ROR) family.

Function

The protein encoded by this gene is a receptor tyrosine kinase that modulates neurite growth in the central nervous system. It is a type I membrane protein and belongs to the ROR subfamily of cell surface receptors.^[5] ROR1 is currently under investigation for its role in the metastasis of cancer cells.^[8]

ROR1 has recently been shown to be expressed on ovarian cancer stem cell, on which it seems to play a functional role in promoting migration/invasion or spheroid formation in vitro and tumor engraftment in immune-deficient mice. Treatment with a humanized mAb specific for ROR1 (UC-961) could inhibit the capacity of ovarian cancer cells to migrate, form spheroids, or engraft immune-deficient mice. Moreover, such treatment inhibited the growth of tumor xenografts, which in turn had a reduced capacity to engraft immune-deficient mice and were relatively depleted of cells with features of CSC, suggesting that treatment with UC-961 could impair CSC renewal. Collectively, these studies indicate that ovarian CSCs express ROR1, which may be targeted for anti-CSC therapy.^[9]

Zilovertamab vedotin (ZV), an antibody–drug conjugate comprising a monoclonal antibody recognizing extracellular ROR1, a cleavable linker and monomethyl auristatin E has entered clinical trials for the treatment of lymphoid malignancies.^[10]

References

Further reading

This article incorporates text from the United States National Library of Medicine, which is in the public domain.

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