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

Verheyen, Esther M

2022 Volume 15, Issue 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 term(s)	Animals ; Drosophila ; Drosophila melanogaster/genetics ; Humans
Language	English
Publishing date	2022-03-29
Publishing country	England
Document type	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
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The power of Drosophila in modeling human disease mechanisms

Esther M. Verheyen

Disease Models & Mechanisms, Vol 15, Iss

2022 Volume 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.
Keywords	Medicine ; R ; Pathology ; RB1-214
Subject code	001
Language	English
Publishing date	2022-03-01T00:00:00Z
Publisher	The Company of Biologists
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: 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 Volume 11, Page(s) 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
Language	English
Publishing date	2023-10-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2023.1214539
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Article ; Online: Metabolic reprogramming in cancer: mechanistic insights from Drosophila.

Wong, Kenneth Kin Lam / Verheyen, Esther M

Disease models & mechanisms

2021 Volume 14, Issue 7, Page(s) 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 term(s)	Animals ; Drosophila ; Glycolysis ; Mitochondria/metabolism ; Neoplasms/pathology ; Oxidative Phosphorylation
Language	English
Publishing date	2021-07-09
Publishing country	England
Document type	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
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Article ; Online: Metabolic reprogramming in cancer

Kenneth Kin Lam Wong / Esther M. Verheyen

Disease Models & Mechanisms, Vol 14, Iss

mechanistic insights from Drosophila

2021 Volume 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 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.
Keywords	aerobic glycolysis ; drosophila cancer models ; metabolic reprogramming ; mitochondria ; Medicine ; R ; Pathology ; RB1-214
Subject code	570
Language	English
Publishing date	2021-07-01T00:00:00Z
Publisher	The Company of Biologists
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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

Wong, Kenneth Kin Lam / Verheyen, Esther M

EMBO reports

2020 Volume 21, Issue 9, Page(s) 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 term(s)	Low Density Lipoprotein Receptor-Related Protein-1 ; Low Density Lipoprotein Receptor-Related Protein-6/genetics ; Neurofibromin 2/genetics ; Neurofibromin 2/metabolism ; Nutrients ; Signal Transduction
Chemical Substances	Low Density Lipoprotein Receptor-Related Protein-1 ; Low Density Lipoprotein Receptor-Related Protein-6 ; Neurofibromin 2
Language	English
Publishing date	2020-08-20
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	2020896-0
ISSN	1469-3178 ; 1469-221X
ISSN (online)	1469-3178
ISSN	1469-221X
DOI	10.15252/embr.202051358
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In stock of ZB MED Cologne/Königswinter

Zs.A 5433: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; 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 Volume 11, Issue 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 term(s)	Animals ; Animals, Genetically Modified ; Drosophila melanogaster/genetics ; Drosophila melanogaster/metabolism ; Gene Expression Regulation, Developmental ; Homeodomain Proteins/metabolism ; Humans ; Phosphorylation ; Protein Kinases/metabolism
Chemical Substances	Homeodomain Proteins ; Protein Kinases (EC 2.7.-)
Language	English
Publishing date	2021-11-30
Publishing country	England
Document type	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
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Article ; 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 Volume 16, Issue 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 term(s)	Animals ; Humans ; Chickens/metabolism ; Craniofacial Abnormalities/genetics ; Dishevelled Proteins/genetics ; Dishevelled Proteins/metabolism ; Drosophila ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Wnt Signaling Pathway/genetics
Chemical Substances	Dishevelled Proteins ; Phosphoproteins
Language	English
Publishing date	2023-04-13
Publishing country	England
Document type	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
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Article ; 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 Volume 123, Page(s) 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 term(s)	Animals ; Disease ; Embryonic Development ; Homeodomain Proteins/metabolism ; Humans ; Models, Biological ; Protein Kinases/metabolism ; Signal Transduction
Chemical Substances	Homeodomain Proteins ; Protein Kinases (EC 2.7.-)
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1557-8933 ; 0070-2153
ISSN (online)	1557-8933
ISSN	0070-2153
DOI	10.1016/bs.ctdb.2016.10.002
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Article ; Online: A positive feedback loop between Myc and aerobic glycolysis sustains tumor growth in a

Wong, Kenneth Kin Lam / Liao, Jenny Zhe / Verheyen, Esther M

eLife

2019 Volume 8

Abstract: Cancer cells usually exhibit aberrant cell signaling and metabolic reprogramming. However, mechanisms of crosstalk between these processes remain elusive. Here, we show that in an in vivo tumor model expressing ... ...

Abstract	Cancer cells usually exhibit aberrant cell signaling and metabolic reprogramming. However, mechanisms of crosstalk between these processes remain elusive. Here, we show that in an in vivo tumor model expressing oncogenic
MeSH term(s)	Aerobiosis ; Animals ; Cell Proliferation ; DNA-Binding Proteins/metabolism ; Disease Models, Animal ; Drosophila Proteins/metabolism ; Drosophila melanogaster/metabolism ; Feedback, Physiological ; Glucose/metabolism ; Glycolysis/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Organ Specificity ; Protein Kinases/metabolism ; Signal Transduction ; Transcription Factors/metabolism ; Up-Regulation/genetics
Chemical Substances	DNA-Binding Proteins ; Drosophila Proteins ; Myc protein, Drosophila ; Transcription Factors ; Protein Kinases (EC 2.7.-) ; HIPK protein, Drosophila (EC 2.7.11.1) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2019-07-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.46315
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