EVC is a membrane-associated component of the EvC ciliary signaling complex. In association with EVC2, it occupies a specialized region of proximal ciliary membrane and promotes Hedgehog signaling downstream of Smoothened. This signaling contribution supports growth-plate organization and endochondral bone growth. Pathogenic human EVC variants cause Ellis–van Creveld syndrome, with skeletal, dental and cardiac abnormalities.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0001501 skeletal system development | TAS PMID:10700184 Mutations in a new gene in Ellis-van Creveld syndrome and We... | KEEP AS NON CORE | Summary: Retain the human skeletal-development association as a downstream developmental context. Reason: The PMID:10700184 target identity and accessible original abstract are verified: EVC variants segregate with the skeletal dysplasia, including short limbs, short ribs and polydactyly. This supports the broad developmental association but does not define an intrinsic molecular activity of EVC. The complete original body remained inaccessible; the nominal publisher PDF returned HTML. Retain this existing positive TAS context as non-core without inventing an embryonic skeletal assay or a particular step performed by the protein. Supporting Evidence: |
| GO:0003416 endochondral bone growth | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Retain endochondral bone growth as a supported developmental consequence of ciliary signaling. Reason: The actual mouse P57680 donor record is experimentally grounded in PMID:17660199. Its operative Methods/Results use Evc-null mice and native mouse chondrocytes/MEFs: shorter endochondral bones and altered growth-plate zones accompany reduced Ptch1/Gli1 responses, including impaired responses to Smoothened agonist purmorphamine. This establishes a positive signaling contribution in the growth plate, not bone-matrix synthesis or autonomous growth activity. The current term covers the increase in size or mass of endochondral bone. Conserved EVC signaling supports this developmental context, while the primary molecular role is in the ciliary signaling complex. Human assays were not performed in this mouse paper; the inference is retained without asserting functional equivalence of the separate shorter RefSeq products. Propagation Review Root cause: NO FAILURE NON CORE Sources checked: UniProtKB:P57680 SUPPORTS TRANSFER Actual mouse IMP17660199 and original growth-plate/signaling experiments support the conserved developmental context. Supporting Evidence: |
| GO:0003416 endochondral bone growth | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Retain endochondral bone growth as a supported developmental consequence of ciliary signaling. Reason: The actual mouse P57680 donor record is experimentally grounded in PMID:17660199. Its operative Methods/Results use Evc-null mice and native mouse chondrocytes/MEFs: shorter endochondral bones and altered growth-plate zones accompany reduced Ptch1/Gli1 responses, including impaired responses to Smoothened agonist purmorphamine. This establishes a positive signaling contribution in the growth plate, not bone-matrix synthesis or autonomous growth activity. The current term covers the increase in size or mass of endochondral bone. Conserved EVC signaling supports this developmental context, while the primary molecular role is in the ciliary signaling complex. Human assays were not performed in this mouse paper; the inference is retained without asserting functional equivalence of the separate shorter RefSeq products. Propagation Review Root cause: NO FAILURE NON CORE Sources checked: UniProtKB:P57680 SUPPORTS TRANSFER Actual mouse IMP17660199 and original growth-plate/signaling experiments support the conserved developmental context. Supporting Evidence: |
| GO:0005886 plasma membrane | IEA GO_REF:0000044 | MODIFY | Summary: Refine the correct broad plasma-membrane mapping to ciliary membrane. Reason: SL-0039 maps correctly to plasma membrane. Actual PMID:21356043 localization/topology experiments use mouse Evc/Evc2 constructs and native mouse cells. Coexpression supports ciliary membrane localization and an intracellular Evc C terminus; human HEK293 is an expression host for mouse interaction fragments. PMID:24582806 independently places the mouse EVC–EVC2 subcomplex at a restricted proximal ciliary membrane zone. The current human Reactome chain R-HSA-5633051 → EVC2:EVC 5633041 → EVC 5633035 identifies P57679 itself, residues 1–992, with its own ciliary-membrane compartment. This is a human model informed by ortholog evidence, not a human-protein assay. GO:0060170 is the specialized portion of plasma membrane surrounding a cilium; the refinement preserves the source mapping while specifying the supported compartment. Propagation Review Root cause: TERM SCOPING PROBLEM Sources checked: UniProtKB-SubCell:SL-0039 SUPPORTS TRANSFER Correct broad membrane mapping; independent original and target-participant evidence supports ciliary membrane. Proposed replacements: ciliary membrane Supporting Evidence: Reactome:R-HSA-5633051 file:human/EVC/EVC-uniprot.txt |
| GO:0005886 plasma membrane | ISS GO_REF:0000024 | MODIFY | Summary: Refine the mouse-supported plasma-membrane assertion to ciliary membrane. Reason: Current P57680 carries experimental PMID:21356043 plasma-membrane evidence. Actual PMID:21356043 localization/topology experiments use mouse Evc/Evc2 constructs and native mouse cells. Coexpression supports ciliary membrane localization and an intracellular Evc C terminus; human HEK293 is an expression host for mouse interaction fragments. PMID:24582806 independently places the mouse EVC–EVC2 subcomplex at a restricted proximal ciliary membrane zone. The current human Reactome chain R-HSA-5633051 → EVC2:EVC 5633041 → EVC 5633035 identifies P57679 itself, residues 1–992, with its own ciliary-membrane compartment. This is a human model informed by ortholog evidence, not a human-protein assay. The membrane-specific localization is more informative than the parent location and does not imply all products or all cell types have identical distribution. Propagation Review Root cause: TERM SCOPING PROBLEM Sources checked: UniProtKB:P57680 SUPPORTS TRANSFER Actual EXP21356043 is the proximate donor source; its mouse construct and host boundaries were read. Proposed replacements: ciliary membrane Supporting Evidence: Reactome:R-HSA-5633051 file:human/EVC/EVC-uniprot.txt |
| GO:0005929 cilium | IDA PMID:21356043 Evc2 is a positive modulator of Hedgehog signalling that int... | MODIFY | Summary: Refine the supported ciliary localization to ciliary membrane, while retaining the separate evidence-code query. Reason: PMID:21356043 supports ciliary localization in mouse native cells and mouse Evc/Evc2 constructs. Its topology and coexpression experiments, together with the independent human Reactome participant and curated UniProt location, place the conserved membrane-associated role more precisely at the ciliary membrane (GO:0060170). This refinement agrees with the electronic cilium row and retains the positive biological conclusion; it does not reject the experiment. The human IDA attribution remains a separate probable source query because the inspected localization experiments use mouse proteins, while HEK293 is a host for mouse interaction fragments. No replacement evidence code, human assay or equivalence among the separate human products is asserted. Proposed replacements: ciliary membrane |
| GO:0005929 cilium | IEA GO_REF:0000120 | MODIFY | Summary: The broad cilium mapping can be refined to the ciliary membrane. Reason: The combined mouse/SL-0066 sources genuinely support cilia. Actual PMID:21356043 localization/topology experiments use mouse Evc/Evc2 constructs and native mouse cells. Coexpression supports ciliary membrane localization and an intracellular Evc C terminus; human HEK293 is an expression host for mouse interaction fragments. PMID:24582806 independently places the mouse EVC–EVC2 subcomplex at a restricted proximal ciliary membrane zone. The current human Reactome chain R-HSA-5633051 → EVC2:EVC 5633041 → EVC 5633035 identifies P57679 itself, residues 1–992, with its own ciliary-membrane compartment. This is a human model informed by ortholog evidence, not a human-protein assay. Current typed ontology places ciliary membrane within cilium and plasma membrane. The finer term is supported independently; neither generic ciliary staining nor the human host alone establishes membrane topology. Propagation Review Root cause: TERM SCOPING PROBLEM Sources checked: UniProtKB:P57680 SUPPORTS TRANSFER Current mouse IDA21356043 and actual original support ciliary localization. UniProtKB-SubCell:SL-0066 SUPPORTS TRANSFER Correct broad cilium mapping; source-specific membrane evidence supplies the refinement. Proposed replacements: ciliary membrane Supporting Evidence: Reactome:R-HSA-5633051 file:human/EVC/EVC-uniprot.txt |
| GO:0007224 smoothened signaling pathway | IEA GO_REF:0000002 | ACCEPT | Summary: Retain Smoothened-pathway participation alongside the separately supported positive-regulation role. Reason: InterPro IPR026501 is a verified EVC family match with the Smoothened-signaling mapping. Evc-null mouse cells have impaired Smoothened-agonist responses and reduced Hedgehog target-gene output in PMID:17660199. Localization and complex studies place EVC within the proximal ciliary signaling machinery; PMID:24582806 also reports signal-dependent association of the EVC–EVC2 complex with SMO. Together these support participation in the series of signals following SMO activation, as well as a positive effect on signaling. GO:0045880 is not an ancestry-equivalent replacement for GO:0007224, so the pathway assertion is retained rather than displaced. The complex-level interaction is not an isolated EVC–SMO binary-binding or EVC-specific adaptor assay, and the mechanistic constructs are mouse proteins. Propagation Review Root cause: NO FAILURE CORE Sources checked: InterPro:IPR026501 SUPPORTS TRANSFER The actual IPR026501 family match and GO mapping are concordant with Evc-specific pathway-response experiments and complex-level signaling evidence. Participation and positive regulation are both retained; no family-derived enzyme activity is inferred. |
| GO:0007517 muscle organ development | TAS PMID:10700184 Mutations in a new gene in Ellis-van Creveld syndrome and We... | UNDECIDED | Summary: The muscle-organ development assertion cannot be resolved from the accessible source. Reason: PMID:10700184 is the verified EVC disease-discovery paper. Its accessible abstract describes skeletal dysplasia and congenital cardiac malformations, but does not identify a muscle-organ development assay or explain the basis of this specific TAS term. The current GO definition concerns formation and maturation of a muscle organ; a cardiac malformation alone does not resolve that claim. The original full body remains unavailable after bounded publisher/repository searches, and a nominal PDF response is HTML. Preserve the source assertion as UNDECIDED rather than infer that the curator made an error from the abstract or substitute a different developmental process. Supporting Evidence: |
| GO:0036064 ciliary basal body | IEA GO_REF:0000107 | ACCEPT | Summary: Retain basal-body localization with explicit ciliary-base and imaging-resolution limits. Reason: Retain the conserved basal-body/ciliary-base localization. PMID:17660199 reports native mouse Evc staining at the distal basal body/transition-zone region using knockout controls, and PMID:21356043 reports native mouse ciliary-base localization. Curated human UniProt SUBCELLULAR LOCATION and the public HPA EVC record provide independent support: HPA016046 is classified as basal body in ASC52telo, serum-starved hTERT-RPE1 and RPTEC/TERT1 cells. The selected blue/red/green images support ciliary-base puncta but do not independently resolve a basal-body marker channel or incorporation into the microtubule array. The shared antigen matches the 992-, 991- and 535-residue RefSeq products, so the human staining is not product-specific. Nearby EvC-zone membrane localization does not negate this bounded basal-body association; no basal-body assembly or scaffold activity is inferred. The source guide gives the public image and antibody locators; GO_REF:0000052 describes the method, not these target-specific observations. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB:P57680 SUPPORTS TRANSFER Actual IDA17660199 ciliary-base microscopy remains positive; independent human HPA provides corroboration with defined resolution/product limits. Supporting Evidence: file:human/EVC/EVC-uniprot.txt file:human/EVC/EVC-source-guide.md |
| GO:0036064 ciliary basal body | ISS GO_REF:0000024 | ACCEPT | Summary: Retain basal-body localization with explicit ciliary-base and imaging-resolution limits. Reason: Retain the conserved basal-body/ciliary-base localization. PMID:17660199 reports native mouse Evc staining at the distal basal body/transition-zone region using knockout controls, and PMID:21356043 reports native mouse ciliary-base localization. Curated human UniProt SUBCELLULAR LOCATION and the public HPA EVC record provide independent support: HPA016046 is classified as basal body in ASC52telo, serum-starved hTERT-RPE1 and RPTEC/TERT1 cells. The selected blue/red/green images support ciliary-base puncta but do not independently resolve a basal-body marker channel or incorporation into the microtubule array. The shared antigen matches the 992-, 991- and 535-residue RefSeq products, so the human staining is not product-specific. Nearby EvC-zone membrane localization does not negate this bounded basal-body association; no basal-body assembly or scaffold activity is inferred. The source guide gives the public image and antibody locators; GO_REF:0000052 describes the method, not these target-specific observations. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB:P57680 SUPPORTS TRANSFER Actual IDA17660199 ciliary-base microscopy remains positive; independent human HPA provides corroboration with defined resolution/product limits. Supporting Evidence: file:human/EVC/EVC-uniprot.txt file:human/EVC/EVC-source-guide.md |
| GO:0045880 positive regulation of smoothened signaling pathway | IEA GO_REF:0000107 | ACCEPT | Summary: EVC is a positive regulator of Smoothened-dependent signaling. Reason: The actual mouse P57680 donor record is experimentally grounded in PMID:17660199. Its operative Methods/Results use Evc-null mice and native mouse chondrocytes/MEFs: shorter endochondral bones and altered growth-plate zones accompany reduced Ptch1/Gli1 responses, including impaired responses to Smoothened agonist purmorphamine. This establishes a positive signaling contribution in the growth plate, not bone-matrix synthesis or autonomous growth activity. In the actual experiment Ihh expression is retained while downstream pathway readouts and agonist responses are impaired, supporting a positive signaling role rather than simply an association with short limbs. This conserved gene-level inference does not identify EVC as the receptor, establish a specific catalytic activity, or demonstrate identical function of untested human products. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB:P57680 SUPPORTS TRANSFER Current mouse IMP17660199 and actual Evc-null agonist/readout experiments support positive regulation. |
| GO:0045880 positive regulation of smoothened signaling pathway | ISS GO_REF:0000024 | ACCEPT | Summary: EVC is a positive regulator of Smoothened-dependent signaling. Reason: The actual mouse P57680 donor record is experimentally grounded in PMID:17660199. Its operative Methods/Results use Evc-null mice and native mouse chondrocytes/MEFs: shorter endochondral bones and altered growth-plate zones accompany reduced Ptch1/Gli1 responses, including impaired responses to Smoothened agonist purmorphamine. This establishes a positive signaling contribution in the growth plate, not bone-matrix synthesis or autonomous growth activity. In the actual experiment Ihh expression is retained while downstream pathway readouts and agonist responses are impaired, supporting a positive signaling role rather than simply an association with short limbs. This conserved gene-level inference does not identify EVC as the receptor, establish a specific catalytic activity, or demonstrate identical function of untested human products. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB:P57680 SUPPORTS TRANSFER Current mouse IMP17660199 and actual Evc-null agonist/readout experiments support positive regulation. |
| GO:0051216 cartilage development | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Retain cartilage development as a bounded downstream context, using independent functional evidence. Reason: The current rat G3V706 donor assertion is IEP PMID:15278943. Its verified abstract reports Evc mRNA/protein distribution in prehypertrophic and hypertrophic growth-plate chondrocytes; operative full Methods/Results remain unread. Expression alone would not establish participation in cartilage development, and no incorrect-gene or curator-error conclusion is drawn. Independently, actual mouse PMID:17660199 growth-plate histology, spatial Gli1/Ptch1 responses and chondrocyte/MEF Smoothened-agonist experiments connect Evc’s signaling work to endochondral cartilage progression. That supports this existing broad developmental context as non-core, while the rat source alone remains limited. It does not assign cartilage-matrix synthesis or a human cartilage-development assay. Propagation Review Root cause: NO FAILURE NON CORE Sources checked: UniProtKB:G3V706 UNRESOLVED Rat identity and IEP15278943 source verified; abstract expression scope only, original body unread. Independent mouse signaling/growth-plate experiments support the retained non-core context. |
| GO:0060170 ciliary membrane | IBA GO_REF:0000033 | ACCEPT | Summary: Retain the experimentally grounded PAINT ciliary-membrane assertion. Reason: In the actual PTHR16795 tree, human P57679 leaf PTN002497663 descends from PTN000423571. The ungapped target MSA sequence is exactly the current 992-aa sequence. Three positive IBD records and no target-path NOT were found; the ciliary-membrane and plasma-membrane-complex IBDs are at PTN000423571, grounded by mouse Evc and Evc2 experimental annotations. This is an ancestral placement, not a donor-count or pairwise-similarity argument. Actual PMID:21356043 localization/topology experiments use mouse Evc/Evc2 constructs and native mouse cells. Coexpression supports ciliary membrane localization and an intracellular Evc C terminus; human HEK293 is an expression host for mouse interaction fragments. PMID:24582806 independently places the mouse EVC–EVC2 subcomplex at a restricted proximal ciliary membrane zone. The current human Reactome chain R-HSA-5633051 → EVC2:EVC 5633041 → EVC 5633035 identifies P57679 itself, residues 1–992, with its own ciliary-membrane compartment. This is a human model informed by ortholog evidence, not a human-protein assay. No target-specific loss of this localization was established; the distinct external RefSeq records were not treated as equivalent functional products. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN000423571 SUPPORTS TRANSFER Actual ciliary-membrane IBD lies on the exact target ancestry; original mouse complex/localization evidence corroborates the conserved placement. |
| GO:0060170 ciliary membrane | IEA GO_REF:0000120 | ACCEPT | Summary: The combined ortholog and subcellular mapping supports ciliary membrane. Reason: SL-0305 explicitly maps to GO:0060170; current mouse P57680 has IDA24582806 for the same location. Actual PMID:21356043 localization/topology experiments use mouse Evc/Evc2 constructs and native mouse cells. Coexpression supports ciliary membrane localization and an intracellular Evc C terminus; human HEK293 is an expression host for mouse interaction fragments. PMID:24582806 independently places the mouse EVC–EVC2 subcomplex at a restricted proximal ciliary membrane zone. The current human Reactome chain R-HSA-5633051 → EVC2:EVC 5633041 → EVC 5633035 identifies P57679 itself, residues 1–992, with its own ciliary-membrane compartment. This is a human model informed by ortholog evidence, not a human-protein assay. Preserve the distinction between mouse original assays and the current human model. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB:P57680 SUPPORTS TRANSFER Actual IDA24582806 source is mouse EVC/EVC2 localization. UniProtKB-SubCell:SL-0305 SUPPORTS TRANSFER Current exact ciliary-membrane mapping verified. |
| GO:0060170 ciliary membrane | TAS Reactome:R-HSA-5633051 | ACCEPT | Summary: The Reactome EVC participant has its own human ciliary-membrane location. Reason: Actual PMID:21356043 localization/topology experiments use mouse Evc/Evc2 constructs and native mouse cells. Coexpression supports ciliary membrane localization and an intracellular Evc C terminus; human HEK293 is an expression host for mouse interaction fragments. PMID:24582806 independently places the mouse EVC–EVC2 subcomplex at a restricted proximal ciliary membrane zone. The current human Reactome chain R-HSA-5633051 → EVC2:EVC 5633041 → EVC 5633035 identifies P57679 itself, residues 1–992, with its own ciliary-membrane compartment. This is a human model informed by ortholog evidence, not a human-protein assay. Event 5633051 is assembly of EFCAB7:IQCE with EVC2:EVC. EVC is a constituent of the native modeled complex, not the catalyst of a neighboring reaction or the EFCAB7 adaptor. The underlying PMID:24582806 separates stable EVC–EVC2 and EFCAB7–IQCE subcomplexes; no obligatory fixed four-subunit stoichiometry or EVC scaffold MF is inferred. |
| GO:0098797 plasma membrane protein complex | IBA GO_REF:0000033 | ACCEPT | Summary: Retain PAINT-supported membership in a plasma-membrane protein complex. Reason: In the actual PTHR16795 tree, human P57679 leaf PTN002497663 descends from PTN000423571. The ungapped target MSA sequence is exactly the current 992-aa sequence. Three positive IBD records and no target-path NOT were found; the ciliary-membrane and plasma-membrane-complex IBDs are at PTN000423571, grounded by mouse Evc and Evc2 experimental annotations. This is an ancestral placement, not a donor-count or pairwise-similarity argument. Actual PMID:24582806 native mouse NIH/3T3 tandem-affinity purification/co-immunoprecipitation and fractionation distinguish stable EVC–EVC2 from EFCAB7–IQCE subcomplexes; reconstituted EvC constructs in human HEK293T are explicitly mouse. PMID:21356043 provides independent Evc–Evc2 interaction and ciliary-membrane targeting evidence. These support EVC as a constituent of a plasma-membrane protein complex, without transferring EFCAB7 adaptor function or assuming every preparation is a fixed tetramer. The existing complex term is suitable; no unverified EVC-specific GO complex identifier is introduced. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN000423571 SUPPORTS TRANSFER Actual complex IBD and exact target descent are supported by experimentally characterized mouse Evc/Evc2 complex biology. |
| GO:0098797 plasma membrane protein complex | IEA GO_REF:0000107 | ACCEPT | Summary: Retain ortholog-supported plasma-membrane complex membership. Reason: Current mouse P57680 has IDA24582806 for this term. Actual PMID:24582806 native mouse NIH/3T3 tandem-affinity purification/co-immunoprecipitation and fractionation distinguish stable EVC–EVC2 from EFCAB7–IQCE subcomplexes; reconstituted EvC constructs in human HEK293T are explicitly mouse. PMID:21356043 provides independent Evc–Evc2 interaction and ciliary-membrane targeting evidence. These support EVC as a constituent of a plasma-membrane protein complex, without transferring EFCAB7 adaptor function or assuming every preparation is a fixed tetramer. The current human Reactome EVC2:EVC complex contains P57679 itself in ciliary membrane, providing concordant modeled participant evidence. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB:P57680 SUPPORTS TRANSFER Actual mouse IDA24582806 source and operative original complex experiments support the conserved role. |
Loading supporting content…
Download this section (compressed HTML)Q: What EVC-specific molecular step links activated Smoothened to downstream GLI regulation, independently of EVC2 association and EFCAB7–IQCE-dependent positioning?
Q: How do the mouse MEF findings in PMID:21356043—full-length Evc detected in cytoplasmic but not nuclear fractions, with Evc2 detected in both—relate to the independent human HPA016046 nucleoplasmic signal? Which cell, product or antibody-specificity differences explain the observations, and can spatially resolved human imaging distinguish basal-body association from adjacent ciliary membrane?
Q: Which of the separately recorded human products, NP_714928.1 (992 residues, matching P57679), NP_001293019.1 (991 residues) and NP_001293021.1 (535 residues), are expressed, incorporated into the EVC2-associated complex and competent for ciliary signaling?
Q: Is there a muscle-cell-autonomous developmental role for human EVC, distinct from congenital cardiac malformation and broader Hedgehog-dependent developmental effects?
Experiment: In ciliated human cells, compare endogenous EVC loss with matched-expression rescue and interaction-guided EVC variants. Measure EVC2 association, ciliary localization and Smoothened accumulation alongside agonist-dependent GLI1/PTCH1 transcription and GLI processing or localization. Include a downstream GLI bypass control to distinguish pathway position from general cell dysfunction. Advance a specific scaffold, adaptor or catalytic model only after directly testing the proposed step.
Hypothesis: EVC has a signaling contribution that can be experimentally separated from its abundance, EVC2 association and ciliary localization.
Type: Genetic separation of function with localization, interaction and signaling assays
Experiment: Compare HPA016046 staining with endogenous EVC tagging in wild-type and EVC-null human ciliated cells. Resolve basal-body and ciliary-membrane markers separately. Test nuclear localization with fractionation controls and product-resolved detection, explicitly comparing with the mouse MEF result in PMID:21356043, which detected full-length Evc only in the cytoplasmic fraction. A negative result in those mouse cells does not settle the independent human HPA signal. Establish genetic specificity before assigning a nuclear mechanism or an ultrastructural basal-body position.
Hypothesis: Ciliary-base antibody staining may represent proximal membrane, basal-body association or a mixture of product-dependent locations.
Type: Genetic specificity controls and spatially resolved microscopy
Experiment: Establish endogenous transcripts and product-specific peptides before comparing the separately recorded 992-, 991- and 535-residue proteins. Test detected products at matched abundance for EVC2 association, proximal ciliary targeting and Hedgehog-responsive transcription, without assuming that an overexpression phenotype establishes physiological isoform function.
Hypothesis: The shorter human RefSeq products may differ in expression, complex incorporation or signaling competence despite sharing the HPA016046 antigen.
Type: Transcript and product-resolved proteomics with controlled functional rescue
Loading supporting content…
Download this section (compressed HTML)Loading supporting content…
Download this section (compressed HTML)Loading supporting content…
Download this section (compressed HTML)