Functional annotation report: *Drosophila melanogaster* CG31099/Dro14-0 (UniProt Q8IMT2) Falcon Edison Scientific Literature 20 citations 1 artifacts 2026-09-08T18:07:47.067988

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Functional annotation report: Drosophila melanogaster CG31099/Dro14-0 (UniProt Q8IMT2)

Executive conclusion

The gene symbol CG10551 is ambiguous in this context, and literature is limited for this specific protein. The supplied UniProt record associates Q8IMT2 with CG10551, CG31099, Dro14-0, and FlyBase identifier FBgn0051099. Independent literature specifically maps Dro14-0 to CG31099 and classifies it as an ecdysteroid kinase-like (EcKL) gene. I therefore treat Q8IMT2–CG31099–Dro14-0 in D. melanogaster as the defensible research target, while retaining CG10551 only as an unresolved record-level alias. The similarly numbered CG10550 is a different EcKL and must not be conflated with this protein. (scanlan2020identifyingcandidatedetoxification pages 32-35, scanlan2020identifyingcandidatedetoxification pages 61-64, scanlan2020identifyingcandidatedetoxification pages 23-27)

The best current annotation is: CG31099/Dro14-0 encodes an uncharacterized EcKL/kinase-like protein whose depletion produces a preliminary developmental-lethality phenotype. Its physiological substrate, exact reaction, subcellular localization, and pathway remain unknown. It cannot presently be annotated specifically as an ecdysteroid kinase, detoxification kinase, checkpoint kinase, or component of a canonical signaling pathway.

Topic Conclusion Evidence type/strength Source/date
Target identity Target is Drosophila melanogaster protein Q8IMT2, mapped in the supplied UniProt context to CG31099/Dro14-0 and FBgn0051099. Scanlan independently maps Dro14-0 to CG31099. Moderate–strong concordance: supplied database record plus gene-specific literature mapping. UniProt context supplied by user; Scanlan et al., 17 Feb 2020 (scanlan2020identifyingcandidatedetoxification pages 32-35, scanlan2020identifyingcandidatedetoxification pages 23-27)
Alias ambiguity The supplied record also gives CG10551, an unusual alias alongside CG31099. Searches found no literature under CG10551, Q8IMT2, or FBgn0051099; therefore CG10551 should be treated as an unresolved record-level alias and not used to import findings for another protein. CG10550 is a different EcKL and must not be conflated with this target. Unresolved: database-supplied alias without independent literature confirmation. UniProt context supplied by user; Scanlan et al., 17 Feb 2020 (scanlan2020identifyingcandidatedetoxification pages 61-64)
Protein-family assignment CG31099/Dro14-0 is included among D. melanogaster ecdysteroid kinase-like (EcKL) genes. This agrees with the supplied EcKL/PF02958, IPR004119, CHK-kinase-like/IPR015897, and kinase-like-superfamily/IPR011009 assignments. It should not be described as a cytochrome P450. Strong for family membership; computational for domains: independent study classification concordant with profile-based annotations. UniProt context supplied by user; Scanlan et al., 17 Feb 2020 (scanlan2020identifyingcandidatedetoxification pages 61-64, scanlan2020identifyingcandidatedetoxification pages 23-27)
Gene-specific phenotype Ubiquitous RNAi against CG31099/Dro14-0 yielded significantly fewer adult offspring than expected, interpreted as putative developmental lethality. The authors reported that this result was not attributable to the known KK-library tiptop misexpression artifact. Moderate: gene-specific in-vivo RNAi evidence, but not a validated null allele or rescue experiment; off-target or incomplete-knockdown concerns remain. Scanlan et al., 17 Feb 2020 (scanlan2020identifyingcandidatedetoxification pages 32-35, scanlan2020identifyingcandidatedetoxification pages 23-27)
Primary biochemical function No catalytic reaction has been experimentally demonstrated for CG31099/Dro14-0. It is therefore not currently justified to annotate this protein as an ecdysteroid kinase or detoxification enzyme at gene-specific resolution. Unknown: no purified-enzyme, metabolomic, substrate-binding, or genetic-rescue evidence identified. Scanlan et al., 17 Feb 2020 (scanlan2020identifyingcandidatedetoxification pages 32-35, scanlan2020identifyingcandidatedetoxification pages 23-27, scanlan2020identifyingcandidatedetoxification pages 8-11)
Substrate specificity No substrate is known for CG31099/Dro14-0. Phenols, steroids, glucosides, hydroxylated plant/fungal toxins, and products of phase-I hydroxylation or glucosidation are only proposed substrate classes for some EcKLs. Speculative family-level hypothesis; no gene-specific support. Scanlan et al., 17 Feb 2020 (scanlan2020identifyingcandidatedetoxification pages 32-35)
Predicted reaction class EcKL proteins are predicted to use ATP to phosphorylate secondary alcohol groups, but that broad prediction does not establish activity or substrate selectivity for CG31099. Computational/family-level inference. Scanlan et al., 17 Feb 2020 (scanlan2020identifyingcandidatedetoxification pages 8-11)
Family biochemical precedent Silkworm BmEc22K phosphorylates the C22 hydroxyl of ecdysteroids, producing physiologically inactive ecdysteroid-22-phosphates that can be stored in oocytes and later hydrolyzed. This is a precedent from Bombyx mori, not evidence that CG31099 catalyzes the same reaction. Strong biochemical precedent for one family member; non-transferable substrate specificity. Scanlan et al., 17 Feb 2020 (scanlan2020identifyingcandidatedetoxification pages 8-11)
Cellular localization No experimentally supported subcellular localization was identified for CG31099/Dro14-0. A cytosolic location might be compatible with a soluble ATP-dependent enzyme, but it is not established and should not be asserted as annotation. Unknown; any compartment assignment is speculative. Scanlan et al., 17 Feb 2020 (scanlan2020identifyingcandidatedetoxification pages 32-35, scanlan2020identifyingcandidatedetoxification pages 23-27)
Pathway assignment No experimentally supported placement in a canonical signaling, ecdysteroid-metabolism, or xenobiotic-detoxification pathway was identified for CG31099. Developmental RNAi lethality does not by itself identify the affected pathway. Unknown: phenotype without mechanistic pathway evidence. Scanlan et al., 17 Feb 2020 (scanlan2020identifyingcandidatedetoxification pages 32-35, scanlan2020identifyingcandidatedetoxification pages 23-27); FlyBase pathway-curation criteria, Jan 2024 (attrill2024anewexperimental pages 3-5, attrill2024anewexperimental pages 1-3)
EcKL xenobiotic response Across the family, 23 of 51 EcKL genes (45%) were induced in at least one xenobiotic-expression dataset, while 15 of 51 (29%) were induced by the xenobiotic-response regulator CncC. These aggregate results do not show that CG31099 itself was induced. Moderate family-level transcriptomic association; not gene-specific functional proof. Scanlan et al., 17 Feb 2020 (scanlan2020identifyingcandidatedetoxification pages 16-20)
Detoxification candidates 24 of 51 EcKLs (47%) received an integrative detoxification score of at least 3, and the authors estimated that 16–24 EcKL genes may function in detoxification. CG31099 instead appeared among low-scoring, putative developmental/physiological “E-class” candidates. Hypothesis-generating integration of evolutionary, expression, and association data; not biochemical validation. Scanlan et al., 17 Feb 2020 (scanlan2020identifyingcandidatedetoxification pages 32-35, scanlan2020identifyingcandidatedetoxification pages 23-27)
Tissue-level family pattern EcKL genes as a family are often enriched in detoxification-associated tissues, particularly Malpighian tubules and adult midguts; no extractable gene-specific tissue-expression value was established for CG31099. Family-level transcriptomic evidence only. Scanlan et al., 17 Feb 2020 (scanlan2020identifyingcandidatedetoxification pages 61-64, scanlan2020identifyingcandidatedetoxification pages 16-20)
Current annotation context FlyBase distinguishes experimental evidence from computational or high-throughput inference and curates enzyme reactions, pathway membership, expression, and GO annotations separately. Its 2024 pathway resource covered 17 pathways and could label unsupported but plausible members as predicted components; absence of CG31099 from the retrieved material is therefore not proof of biological absence. Authoritative curation framework, not gene-specific evidence. Öztürk-Çolak et al., Feb 2024 (ozturkcolak2024flybaseupdatesto pages 2-3, ozturkcolak2024flybaseupdatesto pages 3-4, ozturkcolak2024flybaseupdatesto pages 1-1); Attrill et al., Jan 2024 (attrill2024anewexperimental pages 26-28, attrill2024anewexperimental pages 1-3)
Best current functional statement CG31099/Dro14-0 is an uncharacterized D. melanogaster EcKL/kinase-like protein required or important for normal development in an RNAi assay. Its exact reaction, substrate, cellular site of action, and pathway remain undetermined. Balanced synthesis: family assignment plus preliminary phenotype; mechanistic function unresolved. UniProt context supplied by user; Scanlan et al., 17 Feb 2020 (scanlan2020identifyingcandidatedetoxification pages 32-35, scanlan2020identifyingcandidatedetoxification pages 23-27, scanlan2020identifyingcandidatedetoxification pages 8-11)

Table: Evidence-tier summary separating gene-specific findings for Q8IMT2/CG31099/Dro14-0 from EcKL-family hypotheses and silkworm precedent. It highlights the unresolved CG10551 alias and major mechanistic knowledge gaps.

1. Identity and domain verification

Organism and identifier

The intended organism is correctly specified as Drosophila melanogaster. The directly relevant study analyzed the D. melanogaster EcKL family and explicitly included CG31099 under the name Dro14-0, independently supporting the supplied organism and CG31099/Dro14-0 mapping. Searches under Q8IMT2, CG10551, and FBgn0051099 did not retrieve gene-specific papers, so those identifiers provide no independent literature confirmation beyond the supplied record. (scanlan2020identifyingcandidatedetoxification pages 61-64, scanlan2020identifyingcandidatedetoxification pages 23-27)

Domain and family interpretation

The supplied assignments—EcKL/PF02958, InterPro IPR004119, CHK-kinase-like IPR015897, and kinase-like-domain superfamily IPR011009—are concordant with the literature’s placement of CG31099/Dro14-0 in the EcKL family. “CHK kinase-like,” however, describes structural/domain similarity; it is not evidence that the protein is a canonical Chk1/Chk2 checkpoint kinase or that it phosphorylates protein substrates in DNA-damage signaling.

EcKL proteins are a poorly characterized kinase-like family proposed to use ATP to phosphorylate secondary-alcohol groups on small molecules. This is a family-level functional prediction, not a demonstrated activity of CG31099. (scanlan2020identifyingcandidatedetoxification pages 8-11)

2. Primary molecular function and catalytic reaction

What is established for CG31099

No purified-protein assay, reaction product, substrate-binding experiment, metabolomic perturbation, enzyme-kinetic measurement, catalytic-residue test, or substrate-dependent genetic rescue was found for CG31099/Dro14-0. Consequently:

Family-level biochemical model

The broad proposed EcKL reaction is approximately:

ATP + small-molecule alcohol → ADP + small-molecule phosphate ester.

Potential substrates proposed for some EcKLs include phenols, steroids, glucosides, hydroxylated plant or fungal toxins, and hydroxylated or glucosylated metabolites generated by other detoxification reactions. These are candidate chemical classes rather than CG31099 substrates. (scanlan2020identifyingcandidatedetoxification pages 32-35, scanlan2020identifyingcandidatedetoxification pages 8-11)

The principal experimentally characterized family precedent is silkworm BmEc22K, which phosphorylates the C22 hydroxyl of ecdysteroids to generate physiologically inactive ecdysteroid-22-phosphates. These conjugates are associated with oocyte/yolk storage and can be hydrolyzed after fertilization to release active hormone. The authors emphasized that substrates had not been identified for the other EcKL proteins considered. BmEc22K therefore supports the plausibility of small-molecule alcohol phosphorylation by the family but does not justify transferring ecdysteroid specificity to CG31099. (scanlan2020identifyingcandidatedetoxification pages 8-11)

3. Biological role and phenotype

The only direct gene-specific functional evidence located was ubiquitous RNAi depletion. Knockdown of CG31099/Dro14-0 yielded significantly fewer adult offspring than expected, interpreted as putative developmental lethality. The study reported that this result was not explained by the known tiptop-misexpression artifact affecting some KK RNAi stocks. (scanlan2020identifyingcandidatedetoxification pages 23-27)

This result indicates that normal CG31099 expression may be important during development, but its evidential strength is moderate rather than definitive. RNAi can be incomplete or have off-target effects, and the study did not report validation with an independent null allele, multiple non-overlapping RNAi constructs, transgenic rescue, or stage-resolved phenotyping. The authors accordingly treated CG31099 as a strong candidate for an “E-class” developmental or endogenous physiological EcKL rather than as a high-scoring detoxification candidate. (scanlan2020identifyingcandidatedetoxification pages 32-35)

The phenotype does not reveal whether the proximate defect concerns hormone metabolism, intermediary metabolism, detoxification, cell signaling, or another process. “Developmental lethality” should therefore be recorded as a phenotype, not converted into a mechanistic pathway annotation.

4. Expression, localization, and site of action

CG31099 appears in an EcKL expression heatmap, confirming its inclusion in the analyzed family, but the retrievable text did not provide gene-specific expression values or establish enrichment in a particular tissue, sex, or life stage. It is therefore inappropriate to assign CG31099 specifically to midgut, Malpighian tubule, ovary, or another organ from the family-level analysis. (scanlan2020identifyingcandidatedetoxification pages 61-64)

No experimentally supported subcellular localization was identified. In particular, there is no cited microscopy, fractionation, organelle-proteomics, secretion, or membrane-topology result for CG31099. A soluble intracellular localization might be compatible with an ATP-dependent small-molecule kinase, but that remains inference rather than annotation.

FlyBase’s 2024 update describes current integration of single-cell RNA-sequencing data and cell-type expression summaries into Gene Reports. Such resources are useful for generating localization hypotheses, but expression in a cell type would still not establish the compartment in which the protein acts or its biochemical substrate. (ozturkcolak2024flybaseupdatesto pages 2-3, ozturkcolak2024flybaseupdatesto pages 1-1)

5. Biochemical and signaling pathways

No experimentally supported placement of CG31099 was found in a canonical signaling pathway, ecdysteroid pathway, or xenobiotic-detoxification pathway. The EcKL domain makes small-molecule phosphorylation plausible, while the RNAi phenotype suggests an endogenous developmental requirement, but these observations do not identify a pathway.

This conservative interpretation is consistent with FlyBase’s current pathway-curation framework. Its 2024 resource systematically curated 17 Drosophila pathways using experimentally supported Gene Ontology annotations, distinguished core components from regulators, and could label plausible components lacking fly experiments as predicted rather than experimentally established. It also excluded indirect or overly broad phenotypic effects from pathway-specific claims. (attrill2024anewexperimental pages 3-5, attrill2024anewexperimental pages 26-28, attrill2024anewexperimental pages 1-3)

Accordingly, CG31099 should presently be listed as:

6. EcKL-family statistics and their limits

Scanlan and colleagues analyzed 51 D. melanogaster EcKL genes. Across the family, 23/51 (45%) were induced in at least one xenobiotic-expression dataset and 15/51 (29%) were induced by CncC, a regulator of xenobiotic responses. EcKL genes also showed family-level enrichment in detoxification-associated tissues, particularly adult midguts and Malpighian tubules. None of these aggregate observations establishes the corresponding behavior for CG31099. (scanlan2020identifyingcandidatedetoxification pages 16-20)

Using an integrative score based on evolutionary instability, expression, induction, and related evidence, 24/51 EcKLs (47%) scored at least 3, and the investigators estimated that 16–24 family members might participate in detoxification. CG31099 was instead discussed among low-scoring EcKLs with a putative developmental phenotype. Thus, the available comparative analysis weighs against presenting detoxification as CG31099’s primary established function. (scanlan2020identifyingcandidatedetoxification pages 32-35, scanlan2020identifyingcandidatedetoxification pages 23-27)

7. Recent developments, 2023–2024

No 2023–2024 primary study specifically characterizing Q8IMT2/CG31099/Dro14-0 was identified. The most relevant recent advances are infrastructural rather than mechanistic:

  1. FlyBase update—February 2024. FlyBase expanded cell-type expression displays, GO summaries, enzyme-reaction presentation, and distinctions among experimental, computational, and high-throughput annotations. The article notes that FlyBase contains over 130,000 GO annotations and uses targeted reviews, so absence of a detailed annotation for one gene is not proof that the gene lacks biological function. [Öztürk-Çolak et al., Genetics 227, 2024; DOI/URL: https://doi.org/10.1093/genetics/iyad211] (ozturkcolak2024flybaseupdatesto pages 2-3, ozturkcolak2024flybaseupdatesto pages 3-4, ozturkcolak2024flybaseupdatesto pages 1-1)

  2. Evidence-weighted pathway curation—January 2024. FlyBase introduced systematic experimental-evidence weighting for 17 signaling pathways, including supporting-publication counts and separation of demonstrated from predicted components. This framework reinforces why an RNAi lethality phenotype alone should not be converted into pathway membership. [Attrill et al., Development 151, 2024; DOI/URL: https://doi.org/10.1242/dev.202255] (attrill2024anewexperimental pages 3-5, attrill2024anewexperimental pages 26-28, attrill2024anewexperimental pages 1-3)

The direct CG31099 evidence remains the 2020 EcKL-family preprint: [Scanlan et al., bioRxiv, posted 17 February 2020; DOI/URL: https://doi.org/10.1101/2020.02.17.951962]. Its conclusions are hypothesis-generating because it integrates comparative genomics, published transcriptomes, association data, and RNAi rather than directly determining CG31099 biochemistry. (scanlan2020identifyingcandidatedetoxification pages 32-35, scanlan2020identifyingcandidatedetoxification pages 23-27, scanlan2020identifyingcandidatedetoxification pages 16-20, scanlan2020identifyingcandidatedetoxification pages 8-11)

Defensible current annotation

CG31099/Dro14-0 encodes a poorly characterized EcKL/kinase-like protein in Drosophila melanogaster. Gene-specific RNAi evidence suggests that it is required for normal development. Its physiological reaction, substrate, subcellular localization, and pathway are unknown. EcKL-family membership predicts possible ATP-dependent phosphorylation of a small-molecule alcohol, but neither ecdysteroid nor xenobiotic specificity has been demonstrated.

Highest-value experiments

The most decisive next steps would be: (1) establish a CRISPR null allele and rescue it with a wild-type genomic transgene; (2) define the lethal stage and affected tissues using conditional or tissue-specific depletion; (3) tag the endogenous protein for localization; (4) compare wild-type and null metabolomes, emphasizing phosphorylated steroids and other alcohol-containing metabolites; and (5) assay purified protein against a chemically diverse substrate panel with ATP-consumption and product-confirmation mass spectrometry. Mutation of predicted ATP-binding or catalytic residues followed by biochemical testing and in-vivo rescue would distinguish catalytic from noncatalytic roles.

Final assessment

CG31099/Dro14-0 is a genuine D. melanogaster EcKL-family target consistent with Q8IMT2’s supplied domain annotation, but CG10551 remains an ambiguous alias and should not be used to merge unrelated literature. Evidence currently supports family membership and a preliminary developmental requirement—not a defined enzyme reaction. The substrate, cellular compartment, and pathway requested for functional annotation remain open research questions, and assigning ecdysteroid kinase or detoxification activity would exceed the available evidence.

References

  1. (scanlan2020identifyingcandidatedetoxification pages 32-35): Jack L. Scanlan, Rebecca S. Gledhill-Smith, Paul Battlay, and Charles Robin. Identifying candidate detoxification genes in the ecdysteroid kinase-like (eckl) and cytochrome p450 gene families in drosophila melanogaster by integrating evolutionary and transcriptomic data. bioRxiv, Feb 2020. URL: https://doi.org/10.1101/2020.02.17.951962, doi:10.1101/2020.02.17.951962. This article has 3 citations.

  2. (scanlan2020identifyingcandidatedetoxification pages 61-64): Jack L. Scanlan, Rebecca S. Gledhill-Smith, Paul Battlay, and Charles Robin. Identifying candidate detoxification genes in the ecdysteroid kinase-like (eckl) and cytochrome p450 gene families in drosophila melanogaster by integrating evolutionary and transcriptomic data. bioRxiv, Feb 2020. URL: https://doi.org/10.1101/2020.02.17.951962, doi:10.1101/2020.02.17.951962. This article has 3 citations.

  3. (scanlan2020identifyingcandidatedetoxification pages 23-27): Jack L. Scanlan, Rebecca S. Gledhill-Smith, Paul Battlay, and Charles Robin. Identifying candidate detoxification genes in the ecdysteroid kinase-like (eckl) and cytochrome p450 gene families in drosophila melanogaster by integrating evolutionary and transcriptomic data. bioRxiv, Feb 2020. URL: https://doi.org/10.1101/2020.02.17.951962, doi:10.1101/2020.02.17.951962. This article has 3 citations.

  4. (scanlan2020identifyingcandidatedetoxification pages 8-11): Jack L. Scanlan, Rebecca S. Gledhill-Smith, Paul Battlay, and Charles Robin. Identifying candidate detoxification genes in the ecdysteroid kinase-like (eckl) and cytochrome p450 gene families in drosophila melanogaster by integrating evolutionary and transcriptomic data. bioRxiv, Feb 2020. URL: https://doi.org/10.1101/2020.02.17.951962, doi:10.1101/2020.02.17.951962. This article has 3 citations.

  5. (attrill2024anewexperimental pages 3-5): Helen Attrill, Giulia Antonazzo, Joshua L. Goodman, Jim Thurmond, Victor B Strelets, and Nicholas H. Brown. A new experimental evidence-weighted signaling pathway resource in flybase. Development (Cambridge, England), Jan 2024. URL: https://doi.org/10.1242/dev.202255, doi:10.1242/dev.202255. This article has 3 citations.

  6. (attrill2024anewexperimental pages 1-3): Helen Attrill, Giulia Antonazzo, Joshua L. Goodman, Jim Thurmond, Victor B Strelets, and Nicholas H. Brown. A new experimental evidence-weighted signaling pathway resource in flybase. Development (Cambridge, England), Jan 2024. URL: https://doi.org/10.1242/dev.202255, doi:10.1242/dev.202255. This article has 3 citations.

  7. (scanlan2020identifyingcandidatedetoxification pages 16-20): Jack L. Scanlan, Rebecca S. Gledhill-Smith, Paul Battlay, and Charles Robin. Identifying candidate detoxification genes in the ecdysteroid kinase-like (eckl) and cytochrome p450 gene families in drosophila melanogaster by integrating evolutionary and transcriptomic data. bioRxiv, Feb 2020. URL: https://doi.org/10.1101/2020.02.17.951962, doi:10.1101/2020.02.17.951962. This article has 3 citations.

  8. (ozturkcolak2024flybaseupdatesto pages 2-3): Arzu Öztürk-Çolak, Steven J Marygold, Giulia Antonazzo, Helen Attrill, Damien Goutte-Gattat, Victoria K Jenkins, Beverley B Matthews, Gillian Millburn, Gilberto dos Santos, Christopher J Tabone, Norbert Perrimon, Susan Russo Gelbart, Kris Broll, Madeline Crosby, Gilberto dos Santos, Kathleen Falls, L Sian Gramates, Victoria K Jenkins, Ian Longden, Beverley B Matthews, Jolene Seme, Christopher J Tabone, Pinglei Zhou, Mark Zytkovicz, Nick Brown, Giulia Antonazzo, Helen Attrill, Damien Goutte-Gattat, Aoife Larkin, Steven Marygold, Alex McLachlan, Gillian Millburn, Clare Pilgrim, Arzu Öztürk-Çolak, Thomas Kaufman, Brian Calvi, Seth Campbell, Josh Goodman, Victor Strelets, Jim Thurmond, Richard Cripps, and TyAnna Lovato. Flybase: updates to the drosophila genes and genomes database. Genetics, Feb 2024. URL: https://doi.org/10.1093/genetics/iyad211, doi:10.1093/genetics/iyad211. This article has 479 citations and is from a domain leading peer-reviewed journal.

  9. (ozturkcolak2024flybaseupdatesto pages 3-4): Arzu Öztürk-Çolak, Steven J Marygold, Giulia Antonazzo, Helen Attrill, Damien Goutte-Gattat, Victoria K Jenkins, Beverley B Matthews, Gillian Millburn, Gilberto dos Santos, Christopher J Tabone, Norbert Perrimon, Susan Russo Gelbart, Kris Broll, Madeline Crosby, Gilberto dos Santos, Kathleen Falls, L Sian Gramates, Victoria K Jenkins, Ian Longden, Beverley B Matthews, Jolene Seme, Christopher J Tabone, Pinglei Zhou, Mark Zytkovicz, Nick Brown, Giulia Antonazzo, Helen Attrill, Damien Goutte-Gattat, Aoife Larkin, Steven Marygold, Alex McLachlan, Gillian Millburn, Clare Pilgrim, Arzu Öztürk-Çolak, Thomas Kaufman, Brian Calvi, Seth Campbell, Josh Goodman, Victor Strelets, Jim Thurmond, Richard Cripps, and TyAnna Lovato. Flybase: updates to the drosophila genes and genomes database. Genetics, Feb 2024. URL: https://doi.org/10.1093/genetics/iyad211, doi:10.1093/genetics/iyad211. This article has 479 citations and is from a domain leading peer-reviewed journal.

  10. (ozturkcolak2024flybaseupdatesto pages 1-1): Arzu Öztürk-Çolak, Steven J Marygold, Giulia Antonazzo, Helen Attrill, Damien Goutte-Gattat, Victoria K Jenkins, Beverley B Matthews, Gillian Millburn, Gilberto dos Santos, Christopher J Tabone, Norbert Perrimon, Susan Russo Gelbart, Kris Broll, Madeline Crosby, Gilberto dos Santos, Kathleen Falls, L Sian Gramates, Victoria K Jenkins, Ian Longden, Beverley B Matthews, Jolene Seme, Christopher J Tabone, Pinglei Zhou, Mark Zytkovicz, Nick Brown, Giulia Antonazzo, Helen Attrill, Damien Goutte-Gattat, Aoife Larkin, Steven Marygold, Alex McLachlan, Gillian Millburn, Clare Pilgrim, Arzu Öztürk-Çolak, Thomas Kaufman, Brian Calvi, Seth Campbell, Josh Goodman, Victor Strelets, Jim Thurmond, Richard Cripps, and TyAnna Lovato. Flybase: updates to the drosophila genes and genomes database. Genetics, Feb 2024. URL: https://doi.org/10.1093/genetics/iyad211, doi:10.1093/genetics/iyad211. This article has 479 citations and is from a domain leading peer-reviewed journal.

  11. (attrill2024anewexperimental pages 26-28): Helen Attrill, Giulia Antonazzo, Joshua L. Goodman, Jim Thurmond, Victor B Strelets, and Nicholas H. Brown. A new experimental evidence-weighted signaling pathway resource in flybase. Development (Cambridge, England), Jan 2024. URL: https://doi.org/10.1242/dev.202255, doi:10.1242/dev.202255. This article has 3 citations.

Artifacts

Citations

  1. scanlan2020identifyingcandidatedetoxification pages 61-64
  2. scanlan2020identifyingcandidatedetoxification pages 32-35
  3. scanlan2020identifyingcandidatedetoxification pages 8-11
  4. scanlan2020identifyingcandidatedetoxification pages 16-20
  5. scanlan2020identifyingcandidatedetoxification pages 23-27
  6. attrill2024anewexperimental pages 3-5
  7. attrill2024anewexperimental pages 1-3
  8. ozturkcolak2024flybaseupdatesto pages 2-3
  9. ozturkcolak2024flybaseupdatesto pages 3-4
  10. ozturkcolak2024flybaseupdatesto pages 1-1
  11. attrill2024anewexperimental pages 26-28
  12. Öztürk-Çolak et al., Genetics 227, 2024; DOI/URL: https://doi.org/10.1093/genetics/iyad211
  13. Attrill et al., Development 151, 2024; DOI/URL: https://doi.org/10.1242/dev.202255
  14. Scanlan et al., bioRxiv, posted 17 February 2020; DOI/URL: https://doi.org/10.1101/2020.02.17.951962
  15. https://doi.org/10.1093/genetics/iyad211]
  16. https://doi.org/10.1242/dev.202255]
  17. https://doi.org/10.1101/2020.02.17.951962].
  18. https://doi.org/10.1101/2020.02.17.951962,
  19. https://doi.org/10.1242/dev.202255,
  20. https://doi.org/10.1093/genetics/iyad211,