Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Disruption of PCP signaling causes limb morphogenesis and skeletal defects and may underlie Robinow syndrome and brachydactyly type B.

Human molecular genetics - 15 Jan 2011

Wang Bing, Sinha Tanvi, Jiao Kai, Serra Rosa, Wang Jianbo

Abstract excerpt

Brachydactyly type B (BDB1) and Robinow syndrome (RRS) are two skeletal disorders caused by mutations in ROR2, a co-receptor of Wnt5a. Wnt5a/Ror2 can activate multiple branches of non-canonical Wnt signaling, but it is unclear which branch(es) mediates Wnt5a/Ror2 function in limb skeletal development. Here, we provide evidence implicating the planar cell polarity (PCP) pathway as the downstream component of Wnt5a...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Wnt-5a Protein
Share to Bone Morphogenetic Protein 4

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Polarity

Share to Limb Buds

Share to Limb Deformities, Congenital

Share to Receptor Tyrosine Kinase-like Orphan Receptors

Share to Wnt Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 20962035
DOI: 10.1093/hmg/ddq462
PMCID: PMC3031336

Genes

ROR2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Disruption of PCP signaling causes limb morphogenesis and skeletal defects and may underlie Robinow syndrome and brachydactyly type B.PMID 20962035Read ↗

ROR-Family Receptor Tyrosine Kinases.Semantic proximity Read ↗

The mutation ROR2W749X, linked to human BDB, is a recessive mutation in the mouse, causing brachydactyly, mediating patterning of joints and modeling recessive Robinow syndrome.Semantic proximity Read ↗

Non-canonical Wnt5a/Ror2 signaling regulates kidney morphogenesis by controlling intermediate mesoderm extensionSemantic proximity Read ↗

Rbm8a deficiency causes hematopoietic defects by modulating Wnt/PCP signaling.Semantic proximity Read ↗

Abnormal WNT5A Signaling Causes Mandibular Hypoplasia in Robinow Syndrome.Semantic proximity Read ↗

Ror2 knockout mouse as a model for the developmental pathology of autosomal recessive Robinow syndrome.Semantic proximity Read ↗

FRIZZLED 2 regulates limb development by mediating both β-catenin-dependent and independent Wnt signaling pathwaysSemantic proximity Read ↗

Combinatorial signaling through BMP receptor IB and GDF5: shaping of the distal mouse limb and the genetics of distal limb diversity.Semantic proximity Read ↗

Dominant mutations in ROR2, encoding an orphan receptor tyrosine kinase, cause brachydactyly type B.Semantic proximity Read ↗

WNT pathways and upper limb anomalies.Semantic proximity Read ↗

Dysregulated BMP signaling through ACVR1 impairs digit joint development in fibrodysplasia ossificans progressiva (FOP)Semantic proximity Read ↗

Rbm8a deficiency causes hematopoietic defects by modulating Wnt/PCP signalingSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.