ROR1

 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.

ROR1
Identifiers
AliasesROR1, NTRKR1, dJ537F10.1, receptor tyrosine kinase-like orphan receptor 1, receptor tyrosine kinase like orphan receptor 1
External IDsOMIM602336 MGI1347520 HomoloGene3675 GeneCardsROR1
Gene location (Human)
Chromosome 1 (human)
Chr.Chromosome 1 (human)[1]
Chromosome 1 (human)
Genomic location for ROR1
Genomic location for ROR1
Band1p31.3Start63,774,017 bp[1]
End64,181,498 bp[1]
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
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 MbChr 4: 100.1 – 100.44 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

FunctionEdit

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]

This article uses material from the Wikipedia article
 Metasyntactic variable, which is released under the 
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Attribution-ShareAlike 3.0 Unported License
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