PTK7 is a single-pass receptor pseudokinase with seven extracellular immunoglobulin-like domains. It organizes signaling at cell contacts, including Src-dependent control of junctional actomyosin, and contributes to planar cell polarity and tissue morphogenesis. Its kinase-like domain has an occluded nucleotide pocket and lacks the catalytic machinery of an active receptor tyrosine kinase; it does not bind ATP, and phosphotyrosine signaling downstream of PTK7 is carried out by associated active kinases such as Src. In mouse, loss of Ptk7 disrupts neural tube closure, convergent extension, inner-ear hair-cell planar polarity and heart, lung and kidney development. The rat A0A8I6ALM9 gene model retains the seven Ig-like domains, membrane-spanning helix and pseudokinase-domain residues of mouse and human PTK7, but its first 35 residues differ from the conserved signal peptide encoded by the alternative rat model A0A8I6AKN3.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0001736 establishment of planar polarity | ISO GO_REF:0000121 | ACCEPT | Summary: Planar polarity is a defining PTK7 function. The mouse donor row (MGI IMP, PMID:20704721) reports disrupted inner-ear planar cell polarity in Ptk7 chuzhoi mutants, and mammalian cell and auditory-epithelium experiments connect junctional PTK7-Src signaling to polarized actomyosin. Rat Ptk7 is the one-to-one ortholog of mouse Ptk7 and sits with it in PANTHER subfamily PTHR45080:SF21 in the current UniProt record; the receptor and pseudokinase regions are conserved. Supporting Evidence: PMID:20704721 chuzhoi mutants exhibit disruption of planar cell polarity in the inner ear PMID:24703874 PTK7-Src signaling module for spatial regulation of ROCK activity, actomyosin contractility, and epithelial PCP. file:rat/Ptk7/Ptk7-bioinformatics/RESULTS.md | 948 | A | 957 | A | |
| GO:0001822 kidney development | ISO GO_REF:0000121 | KEEP AS NON CORE | Summary: The original mouse screenβs Table 1 reports moderate cystic kidneys in all three examined Ptk7 mutants. This directly supports the kidney-development annotation via the mouse ortholog; it is retained as a tissue-specific non-core phenotype. Supporting Evidence: file:rat/Ptk7/Ptk7-bioinformatics/kidney-table.md Ptk7 | 3 | β | β | 100% | β | β | β |
| GO:0001843 neural tube closure | ISO GO_REF:0000121 | KEEP AS NON CORE | Summary: The original mouse Ptk7 mutation study directly reports failed neural-tube closure. This conserved morphogenetic role is retained as a developmental consequence of PCP signaling. Supporting Evidence: PMID:15229603 disrupts neural tube closure and stereociliary bundle orientation |
| GO:0003281 ventricular septum development | ISO GO_REF:0000121 | KEEP AS NON CORE | Summary: The mouse donor row is an MGI IMP from PMID:25807483, a forward-genetic congenital heart disease screen that recovered a Ptk7 mutant among its WNT/PCP CHD genes. The chuzhoi study independently reports ventricular septal defects in Ptk7 mutant hearts. This is an organismal consequence of PCP signaling, carried with acts_upstream_of_or_within, and is retained as non-core. Supporting Evidence: PMID:25807483 WNT/planar cell polarity (Ptk7,Prickle 1,Fuz) PMID:20704721 Chuzhoi mutants exhibit defects in the heart including double outlet right ventricle (DORV) with a ventricular septal defect (VSD), or parallel arterial trunks. |
| GO:0003401 axis elongation | ISO GO_REF:0000121 | KEEP AS NON CORE | Summary: The mouse donor row (MGI IMP, PMID:20704721) rests on the shortened and kinked body axis of Ptk7 chuzhoi mutants, which the authors attribute to defective convergent extension. This is an organismal consequence of PCP signaling, correctly carried with the acts_upstream_of_or_within qualifier, and is retained as non-core. Supporting Evidence: PMID:20704721 Mutants exhibited a shortening and kinking of the body axis PMID:20704721 We demonstrate that the phenotype of chuzhoi mutant embryos is consistent with a defect in convergent extension, with a broadened midline and reduced rate of increase in the length-to-width ratio of mutant embryos compared to wild-type. |
| GO:0004714 transmembrane receptor protein tyrosine kinase activity | ISO NOT GO_REF:0000121 | ACCEPT | Summary: The annotation explicitly asserts NOT receptor tyrosine kinase activity, and that negation is correct. PTK7 is a receptor pseudokinase. Human structural evidence identifies an occluded ATP site and noncanonical catalytic motifs; the corresponding rat residues are conserved. PTK7-dependent phosphorylation is mediated by associated active kinases such as Src, not intrinsic receptor tyrosine kinase activity. Supporting Evidence: PMID:32619402 ATP binding to PTK7 and ROR2 is prevented by projection of a tyrosine side-chain from the Ξ²5/Ξ±D hinge region file:rat/Ptk7/Ptk7-bioinformatics/RESULTS.md | 948 | A | 957 | A | PMID:24703874 PTK7 interacts with the tyrosine kinase Src and stimulates Src signaling along cell-cell contacts. PMID:15019986 Mouse PTK7 was shown to be phosphorylated neither by itself nor by other protein tyrosine kinases. |
| GO:0004715 non-membrane spanning protein tyrosine kinase activity | IBA GO_REF:0000033 | REMOVE | Summary: This IBA does not come from the PTK7 lineage. PANTHER:PTN001231168 is a node of the non-receptor tyrosine kinase family PTHR24418 (seed: Drosophila Csk, FB:FBgn0262081), and rat Ptk7 reaches it only because the PANTHER 19.0 rat classification file places A0A8I6ALM9 in PTHR24418:SF399 (MATK). Rat Ptk7 has no SH2 or SH3 domain; it has seven Ig-like domains, a transmembrane helix and a PTK7-type pseudokinase domain, and the current UniProt record places it in PTHR45080:SF21 with mouse and human PTK7, neither of which receives this term. The function is also contradicted on the target itself: PTK7 does not bind ATP, mouse PTK7 shows no auto- or trans-phosphorylation, and the rat sequence keeps the human pocket-occluding residues. The PAINT judgment for the Csk node is not disputed; the target was placed in the wrong family. Propagation Review Root cause: PROPAGATION BAD Failure modes: WRONG ORTHOLOG OR PARALOG PSEUDO OR SUBACTIVITY LOSS Sources checked: PANTHER:PTN001231168 SUPPORTS SOURCE BUT NOT TARGET PTHR24418 (Csk/Src/Tec non-receptor tyrosine kinase) node. Rat Ptk7 is attached to it only through the PANTHER 19.0 rat-file placement in PTHR24418:SF399 (MATK); its orthologs mouse Q8BKG3 and human Q13308 are in PTHR45080:SF21 and are not descendants of this node. Rat Ptk7 is also a pseudokinase (occluded ATP pocket, ALG in place of DFG). FB:FBgn0262081 Β· Drosophila Csk SUPPORTS SOURCE BUT NOT TARGET Experimental seed for the node; its active-kinase evidence is not disputed, but Csk is not a PTK7 ortholog. Supporting Evidence: file:rat/Ptk7/Ptk7-bioinformatics/RESULTS-rereview.md Column 4 assignment for A0A8I6ALM9 in PTHR19.0_rat: PTHR24418:SF399 (MEGAKARYOCYTE-ASSOCIATED TYROSINE-PROTEIN KINASE). file:rat/Ptk7/Ptk7-uniprot.txt PTHR45080:SF21; INACTIVE TYROSINE-PROTEIN KINASE 7 PMID:32619402 ATP binding to PTK7 and ROR2 is prevented by projection of a tyrosine side-chain from the Ξ²5/Ξ±D hinge region file:rat/Ptk7/Ptk7-bioinformatics/RESULTS.md | 948 | A | 957 | A | file:rat/Ptk7/Ptk7-uniprot.txt TRANSMEM 714..735 PMID:15019986 Mouse PTK7 was shown to be phosphorylated neither by itself nor by other protein tyrosine kinases. file:rat/Ptk7/Ptk7-deep-research-falcon.md PTK7 is a **pseudokinase**, not an active tyrosine kinase: its altered catalytic motifs and sterically occluded ATP pocket prevent ATP/MgΒ²βΊ binding and phosphotransfer. |
| GO:0005524 ATP binding | ISO NOT GO_REF:0000121 | ACCEPT | Summary: Retain the explicit NOT ATP binding annotation. PTK7 fails to bind ATP in the characterized receptor pseudokinase mechanism. The rat protein retains the human pocket-occluding residues and ALG motif, providing a sequence-supported reason not to transfer ATP binding from active kinase relatives. Supporting Evidence: PMID:32619402 ATP binding to PTK7 and ROR2 is prevented by projection of a tyrosine side-chain from the Ξ²5/Ξ±D hinge region file:rat/Ptk7/Ptk7-bioinformatics/RESULTS.md | 948 | A | 957 | A | PMID:24107129 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. |
| GO:0005886 plasma membrane | IBA GO_REF:0000033 | ACCEPT | Summary: Plasma membrane is correct for PTK7, a single-pass cell-surface receptor that signals at cell contacts, and the term is consistent with the other plasma-membrane rows. The phylogenetic route of this IBA is wrong, however. PANTHER:PTN002521457 is a Src/Tec/Csk node of PTHR24418, reached only because the PANTHER 19.0 rat file places A0A8I6ALM9 in PTHR24418:SF399 (MATK) instead of the PTK7 subfamily PTHR45080:SF21. The term is accepted on the PTK7 evidence, not on this node. For this specific gene model, plasma-membrane insertion with the PTK7 topology would also depend on an N-terminal signal peptide that A0A8I6ALM9 does not encode (the alternative rat model A0A8I6AKN3 does). Propagation Review Root cause: PROPAGATION BAD Failure modes: WRONG ORTHOLOG OR PARALOG Sources checked: PANTHER:PTN002521457 SUPPORTS SOURCE BUT NOT TARGET Src/Tec/Csk-family node of PTHR24418; rat Ptk7 is a descendant only through its PANTHER 19.0 misclassification into PTHR24418:SF399. The plasma-membrane term happens to be true for PTK7 on independent evidence (mouse PTK7 IDA, PMID:20215345; PTK7 junctional studies), so the row is accepted despite the wrong route. Supporting Evidence: PMID:24703874 PTK7 interacts with the tyrosine kinase Src and stimulates Src signaling along cell-cell contacts. file:rat/Ptk7/Ptk7-uniprot.txt TRANSMEM 714..735 file:rat/Ptk7/Ptk7-bioinformatics/RESULTS-rereview.md Column 4 assignment for A0A8I6ALM9 in PTHR19.0_rat: PTHR24418:SF399 (MEGAKARYOCYTE-ASSOCIATED TYROSINE-PROTEIN KINASE). |
| GO:0005886 plasma membrane | IEA GO_REF:0000120 | ACCEPT | Summary: Plasma-membrane localization is supported by the retained receptor topology and mammalian PTK7 cell-contact localization. The less-conserved N-terminal segment is a product-level trafficking caveat, not evidence of a different organelle. Supporting Evidence: PMID:24703874 PTK7 interacts with the tyrosine kinase Src and stimulates Src signaling along cell-cell contacts. file:rat/Ptk7/Ptk7-uniprot.txt TRANSMEM 714..735 |
| GO:0005886 plasma membrane | ISO GO_REF:0000121 | ACCEPT | Summary: The ortholog-based plasma-membrane annotation fits the conserved single-pass receptor architecture and directly observed mammalian cell-contact signaling. Supporting Evidence: PMID:24703874 PTK7 interacts with the tyrosine kinase Src and stimulates Src signaling along cell-cell contacts. file:rat/Ptk7/Ptk7-uniprot.txt TRANSMEM 714..735 |
| GO:0005886 plasma membrane | ISO GO_REF:0000121 | ACCEPT | Summary: This independent orthology annotation identifies the same well-supported receptor compartment. It does not imply an additional molecular activity. Supporting Evidence: PMID:24703874 PTK7 interacts with the tyrosine kinase Src and stimulates Src signaling along cell-cell contacts. file:rat/Ptk7/Ptk7-uniprot.txt TRANSMEM 714..735 |
| GO:0005911 cell-cell junction | IEA GO_REF:0000120 | ACCEPT | Summary: PTK7 organizes Src signaling along cell-cell contacts; junctional localization is directly relevant to its conserved polarity function. Supporting Evidence: PMID:24703874 PTK7 interacts with the tyrosine kinase Src and stimulates Src signaling along cell-cell contacts. PMID:24703874 PTK7-Src signaling module for spatial regulation of ROCK activity, actomyosin contractility, and epithelial PCP. |
| GO:0005911 cell-cell junction | ISO GO_REF:0000121 | ACCEPT | Summary: Cell-contact localization in the mammalian PCP study supports transfer of the cell-cell-junction compartment to the intact rat receptor. Supporting Evidence: PMID:24703874 PTK7 interacts with the tyrosine kinase Src and stimulates Src signaling along cell-cell contacts. file:rat/Ptk7/Ptk7-uniprot.txt TRANSMEM 714..735 |
| GO:0005911 cell-cell junction | ISO GO_REF:0000121 | ACCEPT | Summary: The junctional annotation agrees with the conserved PTK7-Src mechanism and is retained as a core receptor location. Supporting Evidence: PMID:24703874 PTK7 interacts with the tyrosine kinase Src and stimulates Src signaling along cell-cell contacts. PMID:24703874 PTK7-Src signaling module for spatial regulation of ROCK activity, actomyosin contractility, and epithelial PCP. |
| GO:0007507 heart development | ISO GO_REF:0000121 | KEEP AS NON CORE | Summary: The mouse donor row is an MGI IMP from PMID:25807483, which recovered a Ptk7 mutant among the WNT/PCP genes in its congenital heart disease screen; the chuzhoi study independently reports outflow-tract and septal malformations. Heart development is a tissue-level consequence of the receptor mechanism and is retained as non-core. Supporting Evidence: PMID:25807483 WNT/planar cell polarity (Ptk7,Prickle 1,Fuz) PMID:20704721 Chuzhoi mutants exhibit defects in the heart including double outlet right ventricle (DORV) with a ventricular septal defect (VSD), or parallel arterial trunks. |
| GO:0010976 positive regulation of neuron projection development | IEA GO_REF:0000107 | UNDECIDED | Summary: The human donor annotation traces to PMID:17910947, an RNAi screen of retinoic-acid-stimulated SH-SY5Y differentiation. The cached abstract reports the screening design and emphasizes twinfilin-2; it does not list the PTK7-specific data. This does not establish wrong-gene attribution, but the exact PTK7 response cannot be independently assessed without the full screen. Supporting Evidence: PMID:17910947 Phenotype-based screening of differentiating SH-SY5Y cells following retinoic acid (RA) stimulation |
| GO:0010976 positive regulation of neuron projection development | ISO GO_REF:0000121 | UNDECIDED | Summary: The human donor annotation traces to PMID:17910947, an RNAi screen of retinoic-acid-stimulated SH-SY5Y differentiation. The cached abstract reports the screening design and emphasizes twinfilin-2; it does not list the PTK7-specific data. This does not establish wrong-gene attribution, but the exact PTK7 response cannot be independently assessed without the full screen. Propagation Review Root cause: UNRESOLVED Sources checked: UniProtKB:Q13308 Β· human PTK7 UNRESOLVED Human PTK7 IMP from the SH-SY5Y RNAi screen (PMID:17910947); the cached abstract does not show the PTK7-specific result, so the donor evidence could not be assessed. Supporting Evidence: PMID:17910947 Phenotype-based screening of differentiating SH-SY5Y cells following retinoic acid (RA) stimulation |
| GO:0016020 membrane | IEA GO_REF:0000107 | MODIFY | Summary: Membrane localization is correct but unnecessarily broad for a single-pass cell-surface receptor supported at cell contacts. Proposed replacements: plasma membrane Supporting Evidence: PMID:24703874 PTK7 interacts with the tyrosine kinase Src and stimulates Src signaling along cell-cell contacts. file:rat/Ptk7/Ptk7-uniprot.txt TRANSMEM 714..735 |
| GO:0016020 membrane | ISO GO_REF:0000121 | MODIFY | Summary: The ortholog-based generic membrane term can be specified to the plasma membrane on the conserved receptor topology and junctional evidence. Propagation Review Root cause: TERM SCOPING PROBLEM Failure modes: GRANULARITY MISMATCH Sources checked: MGI:MGI:1918711 Β· mouse Ptk7 SUPPORTS TRANSFER Mouse Ptk7 membrane localization transfers; the generic membrane term is merely less specific than plasma membrane. Proposed replacements: plasma membrane Supporting Evidence: PMID:24703874 PTK7 interacts with the tyrosine kinase Src and stimulates Src signaling along cell-cell contacts. file:rat/Ptk7/Ptk7-uniprot.txt TRANSMEM 714..735 |
| GO:0016301 kinase activity | ISO NOT GO_REF:0000121 | ACCEPT | Summary: The NOT kinase activity annotation correctly captures catalytic inactivity. A kinase-like fold does not confer kinase catalysis. The conserved PTK7 pocket blocks ATP binding; Src is the active kinase in the experimentally resolved junctional module. Supporting Evidence: PMID:32619402 ATP binding to PTK7 and ROR2 is prevented by projection of a tyrosine side-chain from the Ξ²5/Ξ±D hinge region file:rat/Ptk7/Ptk7-bioinformatics/RESULTS.md | 948 | A | 957 | A | PMID:24703874 PTK7 interacts with the tyrosine kinase Src and stimulates Src signaling along cell-cell contacts. PMID:15019986 Mouse PTK7 was shown to be phosphorylated neither by itself nor by other protein tyrosine kinases. |
| GO:0016477 cell migration | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: The human donor experiment links membrane PTK7 levels and proteolytic shedding to actin remodeling and cell invasion. The direction depends on the tested condition, but the broad cell-migration role is supported and retained as non-core. Supporting Evidence: PMID:20837484 The enforced expression of membrane PTK7 in cancer cells leads to the actin cytoskeleton reorganization and the inhibition of cell invasion. |
| GO:0016477 cell migration | ISO GO_REF:0000121 | KEEP AS NON CORE | Summary: The human donor experiment links membrane PTK7 levels and proteolytic shedding to actin remodeling and cell invasion. The direction depends on the tested condition, but the broad cell-migration role is supported and retained as non-core. Supporting Evidence: PMID:20837484 The enforced expression of membrane PTK7 in cancer cells leads to the actin cytoskeleton reorganization and the inhibition of cell invasion. |
| GO:0016740 transferase activity | IEA GO_REF:0000104 | REMOVE | Summary: No intrinsic transferase chemistry follows from this inactive kinase fold. Conserved structural defects prevent the ATP-dependent phosphotransfer reaction; activity of an associated Src kinase is not PTK7 transferase activity. Supporting Evidence: PMID:32619402 ATP binding to PTK7 and ROR2 is prevented by projection of a tyrosine side-chain from the Ξ²5/Ξ±D hinge region file:rat/Ptk7/Ptk7-bioinformatics/RESULTS.md | 948 | A | 957 | A | PMID:24703874 PTK7 interacts with the tyrosine kinase Src and stimulates Src signaling along cell-cell contacts. |
| GO:0030036 actin cytoskeleton organization | IEA GO_REF:0000107 | ACCEPT | Summary: Spatial actomyosin organization is directly connected to PTK7-Src-ROCK signaling in mammalian cells and auditory epithelium, making it a core process of the receptor mechanism. Supporting Evidence: PMID:24703874 PTK7-Src signaling module for spatial regulation of ROCK activity, actomyosin contractility, and epithelial PCP. |
| GO:0030036 actin cytoskeleton organization | ISO GO_REF:0000121 | ACCEPT | Summary: The ortholog-based actin-organization term is supported by the direct PTK7 depletion and junctional-contractility results, with preserved rat receptor architecture. Supporting Evidence: PMID:24703874 PTK7-Src signaling module for spatial regulation of ROCK activity, actomyosin contractility, and epithelial PCP. file:rat/Ptk7/Ptk7-bioinformatics/RESULTS.md | 948 | A | 957 | A | |
| GO:0042060 wound healing | ISO GO_REF:0000121 | KEEP AS NON CORE | Summary: The mouse wound-repair paper explicitly tests Ptk7 mutant genetic interactions and reports failed healing. Retain this ortholog-derived tissue response as non-core; it is not inferred merely from a cell-migration phenotype. Supporting Evidence: PMID:20643356 Mice carrying mutant alleles of PCP genes Vangl2, Celsr1, PTK7, and Scrb1, and the transcription factor Grhl3, interact genetically, exhibiting failed wound healing |
| GO:0045198 establishment of epithelial cell apical/basal polarity | ISO GO_REF:0000121 | UNDECIDED | Summary: The mouse donor annotation traces to PMID:15229603. Its accessible abstract establishes planar polarity, whereas the annotated apical-basal axis is distinct. The full text was not accessible for verification; the curator may have inspected additional data, so this is neither removed nor called a mislabeled PCP result. Propagation Review Root cause: UNRESOLVED Sources checked: MGI:MGI:1918711 Β· mouse Ptk7 UNRESOLVED Mouse Ptk7 IMP from PMID:15229603 (abstract-only cache); the abstract supports planar polarity, and the apical-basal polarity data cannot be checked without the full text. Supporting Evidence: PMID:15229603 disrupts neural tube closure and stereociliary bundle orientation |
| GO:0060026 convergent extension | ISO GO_REF:0000121 | KEEP AS NON CORE | Summary: The mouse donor row (MGI IMP, PMID:20704721) rests on the reduced length-to-width ratio and broadened midline of chuzhoi embryos; Lu et al. (PMID:15229603) also showed the Xenopus homolog is required for neural convergent extension. Convergent extension is a tissue-level manifestation of PTK7-dependent PCP signaling and is retained as non-core with the acts_upstream_of_or_within qualifier. Supporting Evidence: PMID:20704721 We demonstrate that the phenotype of chuzhoi mutant embryos is consistent with a defect in convergent extension, with a broadened midline and reduced rate of increase in the length-to-width ratio of mutant embryos compared to wild-type. PMID:15229603 the Xenopus homologue of PTK7 is required for neural convergent extension and neural tube closure |
| GO:0060484 lung-associated mesenchyme development | ISO GO_REF:0000121 | KEEP AS NON CORE | Summary: Ptk7/chuzhoi mutant lung sections directly show thickened interstitial mesenchyme and reduced septation. This supports the specific developmental annotation as a non-core manifestation of the polarity/morphogenesis mechanism. Supporting Evidence: PMID:20704721 thickened interstitial mesenchyme and reduced sepatation in chuzhoi mutants. |
| GO:0060976 coronary vasculature development | ISO GO_REF:0000121 | UNDECIDED | Summary: The mouse donor annotation (MGI IMP) traces to PMID:25807483, a forward-genetic congenital heart disease screen. Correcting an earlier note, the cached full text does name Ptk7 among the recovered WNT/PCP CHD genes, so the curator's paper does assay this gene. The coronary-vessel phenotype itself is not stated in the cached text (it is presumably in the per-line supplementary phenotype tables), and a general morphogenetic role cannot settle this narrower term. Left UNDECIDED rather than accepted or removed. Propagation Review Root cause: UNRESOLVED Sources checked: MGI:MGI:1918711 Β· mouse Ptk7 UNRESOLVED Mouse Ptk7 IMP from the PMID:25807483 congenital heart disease screen; the Ptk7-specific coronary phenotype is not in the cached text. Supporting Evidence: PMID:25807483 WNT/planar cell polarity (Ptk7,Prickle 1,Fuz) PMID:25807483 Here we report findings from a recessive forward genetic screen in fetal mice, showing that cilia and cilia-transduced cell signalling have important roles in the pathogenesis of CHD. |
| GO:0070161 anchoring junction | IEA GO_REF:0000044 | MODIFY | Summary: Junctional PTK7 signaling is established, but the evidence is most directly stated as cell-cell-junction localization rather than assuming a particular anchoring-junction subtype. Proposed replacements: cell-cell junction Supporting Evidence: PMID:24703874 PTK7 interacts with the tyrosine kinase Src and stimulates Src signaling along cell-cell contacts. |
| GO:0071300 cellular response to retinoic acid | IEA GO_REF:0000107 | UNDECIDED | Summary: The human donor annotation traces to PMID:17910947, an RNAi screen of retinoic-acid-stimulated SH-SY5Y differentiation. The cached abstract reports the screening design and emphasizes twinfilin-2; it does not list the PTK7-specific data. This does not establish wrong-gene attribution, but the exact PTK7 response cannot be independently assessed without the full screen. Supporting Evidence: PMID:17910947 Phenotype-based screening of differentiating SH-SY5Y cells following retinoic acid (RA) stimulation |
| GO:0071300 cellular response to retinoic acid | ISO GO_REF:0000121 | UNDECIDED | Summary: The human donor annotation traces to PMID:17910947, an RNAi screen of retinoic-acid-stimulated SH-SY5Y differentiation. The cached abstract reports the screening design and emphasizes twinfilin-2; it does not list the PTK7-specific data. This does not establish wrong-gene attribution, but the exact PTK7 response cannot be independently assessed without the full screen. Propagation Review Root cause: UNRESOLVED Sources checked: UniProtKB:Q13308 Β· human PTK7 UNRESOLVED Human PTK7 IMP from the SH-SY5Y RNAi screen (PMID:17910947); the cached abstract does not show the PTK7-specific result, so the donor evidence could not be assessed. Supporting Evidence: PMID:17910947 Phenotype-based screening of differentiating SH-SY5Y cells following retinoic acid (RA) stimulation |
| GO:0090103 cochlea morphogenesis | ISO GO_REF:0000121 | KEEP AS NON CORE | Summary: The mouse donor row (MGI IMP, PMID:20704721) rests on disrupted hair-cell planar polarity in the chuzhoi cochlear epithelium. Cochlear morphogenesis is a tissue-specific manifestation of the core PCP function, carried with acts_upstream_of_or_within, and retained as non-core. Supporting Evidence: PMID:20704721 chuzhoi mutants exhibit disruption of planar cell polarity in the inner ear PMID:24703874 PTK7-Src signaling module for spatial regulation of ROCK activity, actomyosin contractility, and epithelial PCP. |
| GO:0090263 positive regulation of canonical Wnt signaling pathway | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: The donor experiment directly reports reduced Wnt3a-induced beta-catenin/TCF activity after PTK7 depletion. This supports a positive canonical Wnt role in that setting. Retain the orthology annotation as context-dependent and non-core; conflicting effects in other models do not invalidate the measured positive effect. Supporting Evidence: PMID:21132015 PTK7-deficient cells exhibit weakened Ξ²-catenin/T-cell factor transcriptional activity on Wnt3a stimulation. |
| GO:0090263 positive regulation of canonical Wnt signaling pathway | ISO GO_REF:0000121 | KEEP AS NON CORE | Summary: The donor experiment directly reports reduced Wnt3a-induced beta-catenin/TCF activity after PTK7 depletion. This supports a positive canonical Wnt role in that setting. Retain the orthology annotation as context-dependent and non-core; conflicting effects in other models do not invalidate the measured positive effect. Supporting Evidence: PMID:21132015 PTK7-deficient cells exhibit weakened Ξ²-catenin/T-cell factor transcriptional activity on Wnt3a stimulation. |
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Download this section (compressed HTML)Q: Does the selected rat N-terminal product reach the cell surface with the same efficiency and topology as canonical PTK7?
Q: Which rat Ptk7 5' exon is used in vivo? A0A8I6ALM9 (Ensembl canonical Ptk7-202) lacks the conserved signal peptide that A0A8I6AKN3 (Ptk7-201) and mouse and human PTK7 encode; should the RGD and UniProt gene-centric representative be switched to the signal-peptide-bearing model?
Q: Can PANTHER reclassify rat Ptk7 from PTHR24418:SF399 (MATK) to PTHR45080:SF21, so that rat receives the PTK7-node IBAs (for example PTN000701324, cell-cell junction and regulation of canonical Wnt signaling) instead of Csk/Src-node kinase terms?
Experiment: 5' RACE or long-read cDNA sequencing of rat Ptk7 transcripts from embryonic neural tube and cochlea, with surface biotinylation of epitope-tagged A0A8I6ALM9 and A0A8I6AKN3 products, to establish which N-terminus is expressed and whether the signal-peptide-less product reaches the plasma membrane.
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