Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Electronic Gene Ontology annotations created by transferring manual GO annotations between related proteins based on shared sequence features
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Combined Automated Annotation using Multiple IEA Methods
RGD ISO annotations to rat from other mammalian species
Structural Insights into Pseudokinase Domains of Receptor Tyrosine Kinases.
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Human PTK7 structural analysis identifies a sterically obstructed ATP-binding site; the implicated PTK7 residues are retained in the selected rat sequence.
"ATP binding to PTK7 and ROR2 is prevented by projection of a tyrosine side-chain from the β5/αD hinge region"
PTK7-Src signaling at epithelial cell contacts mediates spatial organization of actomyosin and planar cell polarity.
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Cell experiments show PTK7 recruits or organizes active Src at junctions rather than catalyzing Src-like phosphorylation itself.
"PTK7 interacts with the
tyrosine kinase Src and stimulates Src signaling along cell-cell contacts."
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Cell and mouse auditory-epithelium experiments link junctional PTK7-Src signaling to actomyosin organization and planar polarity.
"PTK7-Src signaling module for spatial regulation of ROCK activity, actomyosin
contractility, and epithelial PCP."
Rat-human PTK7 sequence and structural-landmark mapping
Exact selected rat PTK7 sequence and machine domain features
UniProt record identifying the emitted fly function donor
Frozen exact-input ProtNLM output and UniProt sequence for A0A8I6ALM9
Protein tyrosine kinase 7 has a conserved role in Wnt/β-catenin canonical signalling.
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PTK7 depletion reduces canonical Wnt reporter output in the tested cells; the positive sign is experimentally grounded and context-specific.
"PTK7-deficient cells exhibit weakened β-catenin/T-cell factor transcriptional activity on Wnt3a stimulation."
Epidermal wound repair is regulated by the planar cell polarity signaling pathway.
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Mouse genetic interactions implicate PTK7 in wound repair without establishing an autonomous wound-specific catalytic activity.
"Mice carrying mutant alleles of PCP genes Vangl2,
Celsr1, PTK7, and Scrb1, and the transcription factor Grhl3, interact
genetically, exhibiting failed wound healing"
The novel mouse mutant, chuzhoi, has disruption of Ptk7 protein and exhibits defects in neural tube, heart and lung development and abnormal planar cell polarity in the ear.
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Histology of Ptk7/chuzhoi mutant lungs identifies thickened interstitial mesenchyme and defective septation.
"thickened interstitial mesenchyme and reduced sepatation in chuzhoi mutants."
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Mouse Ptk7/chuzhoi mutants have direct heart and septal developmental phenotypes, independently supporting the corresponding orthology annotations.
"Chuzhoi mutants exhibit defects in the heart including double outlet right ventricle (DORV) with a ventricular septal defect (VSD), or parallel arterial trunks."
PTK7/CCK-4 is a novel regulator of planar cell polarity in vertebrates.
Identification of twinfilin-2 as a factor involved in neurite outgrowth by RNAi-based screen.
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The donor paper is a neuronal RNAi screen; its abstract foregrounds twinfilin-2 and does not enumerate the PTK7 result.
"Phenotype-based screening of differentiating SH-SY5Y cells following
retinoic acid (RA) stimulation"
The Wnt/planar cell polarity protein-tyrosine kinase-7 (PTK7) is a highly efficient proteolytic target of membrane type-1 matrix metalloproteinase: implications in cancer and embryogenesis.
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Human cell experiments connect PTK7 to actin organization and invasion; direction depends on context and receptor shedding.
"The enforced expression of membrane PTK7 in cancer cells
leads to the actin cytoskeleton reorganization and the inhibition of cell
invasion."
Cloning and characterization of the full-length mouse Ptk7 cDNA encoding a defective receptor protein tyrosine kinase.
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Mouse PTK7 shows no auto- or trans-phosphorylation and does not raise cellular phosphotyrosine, the basis of the MGI NOT kinase-activity IDA annotations propagated to rat by ISO.
"Mouse PTK7 was shown to be phosphorylated neither by itself nor by other protein tyrosine kinases."
A robust methodology to subclassify pseudokinases based on their nucleotide-binding properties.
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Thermal-shift profiling classes PTK7 among pseudokinases that do not bind ATP; source of the human NOT ATP binding IDA row propagated to rat.
"CCK4 (colon carcinoma kinase 4)/PTK7 (protein tyrosine kinase 7) [56], BubR1 [35], IRAK3/IRAK-M [57] and MviN [28] were not catalytically active in vitro in previously published studies, consistent with our observations that they do not bind ATP."
Global genetic analysis in mice unveils central role for cilia in congenital heart disease.
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The congenital heart disease screen recovered a Ptk7 mutant line among its WNT/planar cell polarity CHD genes; source of the MGI IMP heart development, ventricular septum development and coronary vasculature development rows.
"WNT/planar cell polarity (Ptk7,Prickle 1,Fuz)"
Falcon deep research report on rat Ptk7 (UniProt A0A8I6ALM9)
Rat Ptk7 gene-model comparison and PANTHER 19.0 classification row (re-review 2026-10-21)
PMID:27002738 Table 1: exact Ptk7 kidney phenotype and headers