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  1. AU=Verheyen Esther M
  2. AU=Katsinelos Panagiotis AU=Katsinelos Panagiotis
  3. AU="Herst, C V"
  4. AU=Wang Lu AU=Wang Lu
  5. AU="Yousif, Yousif"
  6. AU="Songül KARAKAYA"
  7. AU="Bang, Sunghee"
  8. AU="Stasiak, Andrzej"
  9. AU="Ward, B.F.L."
  10. AU="Wu, Sizhu"
  11. AU="Maria-Magdalena Titirici"
  12. AU="Papapoulos, Socrates"
  13. AU="Valdivia, Anddre Osmar"
  14. AU="Graham, Miranda"
  15. AU="Lisitsyn, Nikolai A"

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Treffer 1 - 10 von insgesamt 75

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  1. Artikel ; Online: Solving the Wnt nuclear puzzle.

    Verheyen, Esther M / Gottardi, Cara J

    Nature reviews. Molecular cell biology

    2024  

    Sprache Englisch
    Erscheinungsdatum 2024-05-17
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2031313-5
    ISSN 1471-0080 ; 1471-0072
    ISSN (online) 1471-0080
    ISSN 1471-0072
    DOI 10.1038/s41580-024-00747-7
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: The power of Drosophila in modeling human disease mechanisms.

    Verheyen, Esther M

    Disease models & mechanisms

    2022  Band 15, Heft 3

    Abstract: Six years ago, DMM launched a subject collection called 'Drosophila as a Disease Model'. This collection features Review-type articles and original research that highlight the power of Drosophila research in many aspects of human disease modeling. In the ...

    Abstract Six years ago, DMM launched a subject collection called 'Drosophila as a Disease Model'. This collection features Review-type articles and original research that highlight the power of Drosophila research in many aspects of human disease modeling. In the ensuing years, Drosophila research has further expanded to capitalize on genome editing, development of resources, and further interest in studying rare disease mechanisms. In the current issue of DMM, we again highlight the versatility, breadth, and scope of Drosophila research in human disease modeling and translational medicine. While many researchers have embraced the power of the fly, many more could still be encouraged to appreciate the strengths of Drosophila and how such research can integrate across species in a multi-pronged approach. Only when we truly acknowledge that all models contribute to our understanding of human biology, can we take advantage of the scope of current research endeavors.
    Mesh-Begriff(e) Animals ; Drosophila ; Drosophila melanogaster/genetics ; Humans
    Sprache Englisch
    Erscheinungsdatum 2022-03-29
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2451104-3
    ISSN 1754-8411 ; 1754-8403
    ISSN (online) 1754-8411
    ISSN 1754-8403
    DOI 10.1242/dmm.049549
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: The power of Drosophila in modeling human disease mechanisms

    Esther M. Verheyen

    Disease Models & Mechanisms, Vol 15, Iss

    2022  Band 3

    Abstract: Six years ago, DMM launched a subject collection called ‘Drosophila as a Disease Model’. This collection features Review-type articles and original research that highlight the power of Drosophila research in many aspects of human disease modeling. In the ...

    Abstract Six years ago, DMM launched a subject collection called ‘Drosophila as a Disease Model’. This collection features Review-type articles and original research that highlight the power of Drosophila research in many aspects of human disease modeling. In the ensuing years, Drosophila research has further expanded to capitalize on genome editing, development of resources, and further interest in studying rare disease mechanisms. In the current issue of DMM, we again highlight the versatility, breadth, and scope of Drosophila research in human disease modeling and translational medicine. While many researchers have embraced the power of the fly, many more could still be encouraged to appreciate the strengths of Drosophila and how such research can integrate across species in a multi-pronged approach. Only when we truly acknowledge that all models contribute to our understanding of human biology, can we take advantage of the scope of current research endeavors.
    Schlagwörter Medicine ; R ; Pathology ; RB1-214
    Thema/Rubrik (Code) 001
    Sprache Englisch
    Erscheinungsdatum 2022-03-01T00:00:00Z
    Verlag The Company of Biologists
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel: The AMPK-like protein kinases Sik2 and Sik3 interact with Hipk and induce synergistic tumorigenesis in a

    Yu, Kewei / Ramkumar, Niveditha / Wong, Kenneth Kin Lam / Tettweiler, Gritta / Verheyen, Esther M

    Frontiers in cell and developmental biology

    2023  Band 11, Seite(n) 1214539

    Abstract: Homeodomain-interacting protein kinases (Hipks) regulate cell proliferation, apoptosis, and tissue development. Overexpression of Hipk ... ...

    Abstract Homeodomain-interacting protein kinases (Hipks) regulate cell proliferation, apoptosis, and tissue development. Overexpression of Hipk in
    Sprache Englisch
    Erscheinungsdatum 2023-10-03
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2023.1214539
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Metabolic reprogramming in cancer: mechanistic insights from Drosophila.

    Wong, Kenneth Kin Lam / Verheyen, Esther M

    Disease models & mechanisms

    2021  Band 14, Heft 7, Seite(n) 1–17

    Abstract: Cancer cells constantly reprogram their metabolism as the disease progresses. However, our understanding of the metabolic complexity of cancer remains incomplete. Extensive research in the fruit fly Drosophila has established numerous tumor models ... ...

    Abstract Cancer cells constantly reprogram their metabolism as the disease progresses. However, our understanding of the metabolic complexity of cancer remains incomplete. Extensive research in the fruit fly Drosophila has established numerous tumor models ranging from hyperplasia to neoplasia. These fly tumor models exhibit a broad range of metabolic profiles and varying nutrient sensitivity. Genetic studies show that fly tumors can use various alternative strategies, such as feedback circuits and nutrient-sensing machinery, to acquire and consolidate distinct metabolic profiles. These studies not only provide fresh insights into the causes and functional relevance of metabolic reprogramming but also identify metabolic vulnerabilities as potential targets for cancer therapy. Here, we review the conceptual advances in cancer metabolism derived from comparing and contrasting the metabolic profiles of fly tumor models, with a particular focus on the Warburg effect, mitochondrial metabolism, and the links between diet and cancer.
    Mesh-Begriff(e) Animals ; Drosophila ; Glycolysis ; Mitochondria/metabolism ; Neoplasms/pathology ; Oxidative Phosphorylation
    Sprache Englisch
    Erscheinungsdatum 2021-07-09
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2451104-3
    ISSN 1754-8411 ; 1754-8403
    ISSN (online) 1754-8411
    ISSN 1754-8403
    DOI 10.1242/dmm.048934
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Metabolic reprogramming in cancer

    Kenneth Kin Lam Wong / Esther M. Verheyen

    Disease Models & Mechanisms, Vol 14, Iss

    mechanistic insights from Drosophila

    2021  Band 7

    Abstract: Cancer cells constantly reprogram their metabolism as the disease progresses. However, our understanding of the metabolic complexity of cancer remains incomplete. Extensive research in the fruit fly Drosophila has established numerous tumor models ... ...

    Abstract Cancer cells constantly reprogram their metabolism as the disease progresses. However, our understanding of the metabolic complexity of cancer remains incomplete. Extensive research in the fruit fly Drosophila has established numerous tumor models ranging from hyperplasia to neoplasia. These fly tumor models exhibit a broad range of metabolic profiles and varying nutrient sensitivity. Genetic studies show that fly tumors can use various alternative strategies, such as feedback circuits and nutrient-sensing machinery, to acquire and consolidate distinct metabolic profiles. These studies not only provide fresh insights into the causes and functional relevance of metabolic reprogramming but also identify metabolic vulnerabilities as potential targets for cancer therapy. Here, we review the conceptual advances in cancer metabolism derived from comparing and contrasting the metabolic profiles of fly tumor models, with a particular focus on the Warburg effect, mitochondrial metabolism, and the links between diet and cancer.
    Schlagwörter aerobic glycolysis ; drosophila cancer models ; metabolic reprogramming ; mitochondria ; Medicine ; R ; Pathology ; RB1-214
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2021-07-01T00:00:00Z
    Verlag The Company of Biologists
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  7. Artikel ; Online: LRP6 lets Merlin go in times of nutrient scarcity.

    Wong, Kenneth Kin Lam / Verheyen, Esther M

    EMBO reports

    2020  Band 21, Heft 9, Seite(n) e51358

    Abstract: Cells take advantage of cross-talk in signaling pathways to integrate diverse signals and produce coordinated responses. In this issue of EMBO Reports, Jeong et al discover that the Wnt co-receptor, low-density lipoprotein (LDL) receptor-related protein ... ...

    Abstract Cells take advantage of cross-talk in signaling pathways to integrate diverse signals and produce coordinated responses. In this issue of EMBO Reports, Jeong et al discover that the Wnt co-receptor, low-density lipoprotein (LDL) receptor-related protein LRP6, negatively regulates Hippo signaling by serving as a binding sink to sequester and inhibit Merlin, an activator of Hippo signaling (Jeong et al, 2020). This regulation is nutrient-responsive, likely using LRP6 O-GlcNAcylation as a molecular switch.
    Mesh-Begriff(e) Low Density Lipoprotein Receptor-Related Protein-1 ; Low Density Lipoprotein Receptor-Related Protein-6/genetics ; Neurofibromin 2/genetics ; Neurofibromin 2/metabolism ; Nutrients ; Signal Transduction
    Chemische Substanzen Low Density Lipoprotein Receptor-Related Protein-1 ; Low Density Lipoprotein Receptor-Related Protein-6 ; Neurofibromin 2
    Sprache Englisch
    Erscheinungsdatum 2020-08-20
    Erscheinungsland England
    Dokumenttyp Journal Article ; Comment
    ZDB-ID 2020896-0
    ISSN 1469-3178 ; 1469-221X
    ISSN (online) 1469-3178
    ISSN 1469-221X
    DOI 10.15252/embr.202051358
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: Expression of human HIPKs in Drosophila demonstrates their shared and unique functions in a developmental model.

    Kinsey, Stephen D / Vinluan, Justin P / Shipman, Gerald A / Verheyen, Esther M

    G3 (Bethesda, Md.)

    2021  Band 11, Heft 12

    Abstract: Homeodomain-interacting protein kinases (HIPKs) are a family of four conserved proteins essential for vertebrate development, as demonstrated by defects in the eye, brain, and skeleton that culminate in embryonic lethality when multiple HIPKs are lost in ...

    Abstract Homeodomain-interacting protein kinases (HIPKs) are a family of four conserved proteins essential for vertebrate development, as demonstrated by defects in the eye, brain, and skeleton that culminate in embryonic lethality when multiple HIPKs are lost in mice. While HIPKs are essential for development, functional redundancy between the four vertebrate HIPK paralogues has made it difficult to compare their respective functions. Because understanding the unique and shared functions of these essential proteins could directly benefit the fields of biology and medicine, we addressed the gap in knowledge of the four vertebrate HIPK paralogues by studying them in the fruit fly Drosophila melanogaster, where reduced genetic redundancy simplifies our functional assessment. The single hipk present in the fly allowed us to perform rescue experiments with human HIPK genes that provide new insight into their individual functions not easily assessed in vertebrate models. Furthermore, the abundance of genetic tools and established methods for monitoring specific developmental pathways and gross morphological changes in the fly allowed for functional comparisons in endogenous contexts. We first performed rescue experiments to demonstrate the extent to which each of the human HIPKs can functionally replace Drosophila Hipk for survival and morphological development. We then showed the ability of each human HIPK to modulate Armadillo/β-catenin levels, JAK/STAT activity, proliferation, growth, and death, each of which have previously been described for Hipks, but never all together in comparable tissue contexts. Finally, we characterized novel developmental phenotypes induced by human HIPKs to gain insight to their unique functions. Together, these experiments provide the first direct comparison of all four vertebrate HIPKs to determine their roles in a developmental context.
    Mesh-Begriff(e) Animals ; Animals, Genetically Modified ; Drosophila melanogaster/genetics ; Drosophila melanogaster/metabolism ; Gene Expression Regulation, Developmental ; Homeodomain Proteins/metabolism ; Humans ; Phosphorylation ; Protein Kinases/metabolism
    Chemische Substanzen Homeodomain Proteins ; Protein Kinases (EC 2.7.-)
    Sprache Englisch
    Erscheinungsdatum 2021-11-30
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2629978-1
    ISSN 2160-1836 ; 2160-1836
    ISSN (online) 2160-1836
    ISSN 2160-1836
    DOI 10.1093/g3journal/jkab350
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Mechanistic studies in Drosophila and chicken give new insights into functions of DVL1 in dominant Robinow syndrome.

    Gignac, Sarah J / MacCharles, Katja R / Fu, Katherine / Bonaparte, Kywana / Akarsu, Gamze / Barrett, Thalia W / Verheyen, Esther M / Richman, Joy M

    Disease models & mechanisms

    2023  Band 16, Heft 4

    Abstract: The study of rare genetic diseases provides valuable insights into human gene function. The autosomal dominant or autosomal recessive forms of Robinow syndrome are genetically heterogeneous, and the common theme is that all the mutations lie in genes in ... ...

    Abstract The study of rare genetic diseases provides valuable insights into human gene function. The autosomal dominant or autosomal recessive forms of Robinow syndrome are genetically heterogeneous, and the common theme is that all the mutations lie in genes in Wnt signaling pathways. Cases diagnosed with Robinow syndrome do survive to adulthood with distinct skeletal phenotypes, including limb shortening and craniofacial abnormalities. Here, we focus on mutations in dishevelled 1 (DVL1), an intracellular adaptor protein that is required for both canonical (β-catenin-dependent) or non-canonical (requiring small GTPases and JNK) Wnt signaling. We expressed human wild-type DVL1 or DVL1 variants alongside the endogenous genome of chicken and Drosophila. This design is strategically suited to test for functional differences between mutant and wild-type human proteins in relevant developmental contexts. The expression of variant forms of DVL1 produced a major disorganization of cartilage and Drosophila wing morphology compared to expression of wild-type DVL1. Moreover, the variants caused a loss of canonical and gain of non-canonical Wnt signaling in several assays. Our data point to future therapies that might correct the levels of Wnt signaling, thus improving skeletal growth.
    Mesh-Begriff(e) Animals ; Humans ; Chickens/metabolism ; Craniofacial Abnormalities/genetics ; Dishevelled Proteins/genetics ; Dishevelled Proteins/metabolism ; Drosophila ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Wnt Signaling Pathway/genetics
    Chemische Substanzen Dishevelled Proteins ; Phosphoproteins
    Sprache Englisch
    Erscheinungsdatum 2023-04-13
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2451104-3
    ISSN 1754-8411 ; 1754-8403
    ISSN (online) 1754-8411
    ISSN 1754-8403
    DOI 10.1242/dmm.049844
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: Homeodomain-Interacting Protein Kinases: Diverse and Complex Roles in Development and Disease.

    Blaquiere, Jessica A / Verheyen, Esther M

    Current topics in developmental biology

    2017  Band 123, Seite(n) 73–103

    Abstract: The Homeodomain-interacting protein kinase (Hipk) family of proteins plays diverse, and at times conflicting, biological roles in normal development and disease. In this review we will highlight developmental and cellular roles for Hipk proteins, with an ...

    Abstract The Homeodomain-interacting protein kinase (Hipk) family of proteins plays diverse, and at times conflicting, biological roles in normal development and disease. In this review we will highlight developmental and cellular roles for Hipk proteins, with an emphasis on the pleiotropic and essential physiological roles revealed through genetic studies. We discuss the myriad ways of regulating Hipk protein function, and how these may contribute to the diverse cellular roles. Furthermore we will describe the context-specific activities of Hipk family members in diseases such as cancer and fibrosis, including seemingly contradictory tumor-suppressive and oncogenic activities. Given the diverse signaling pathways regulated by Hipk proteins, it is likely that Hipks act to fine-tune signaling and may mediate cross talk in certain contexts. Such regulation is emerging as vital for development and in disease.
    Mesh-Begriff(e) Animals ; Disease ; Embryonic Development ; Homeodomain Proteins/metabolism ; Humans ; Models, Biological ; Protein Kinases/metabolism ; Signal Transduction
    Chemische Substanzen Homeodomain Proteins ; Protein Kinases (EC 2.7.-)
    Sprache Englisch
    Erscheinungsdatum 2017
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Review
    ISSN 1557-8933 ; 0070-2153
    ISSN (online) 1557-8933
    ISSN 0070-2153
    DOI 10.1016/bs.ctdb.2016.10.002
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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