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  1. AU=Wickenden Julie A
  2. AU="Darbes, Lynae A"
  3. AU="Ostermann, Philipp"
  4. AU="Qiu, Y Z"
  5. AU="Luo, Yue-Jia"
  6. AU="Tamandl, Dietmar" AU="Tamandl, Dietmar"
  7. AU="Holzer, Timothy R"
  8. AU="Zhou, C L"
  9. AU="Lomax, Tony"

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  1. Artikel ; Online: Key signalling nodes in mammary gland development and cancer. Signalling downstream of PI3 kinase in mammary epithelium: a play in 3 Akts.

    Wickenden, Julie A / Watson, Christine J

    Breast cancer research : BCR

    2010  Band 12, Heft 2, Seite(n) 202

    Abstract: The protein serine/threonine kinase Akt, also known as protein kinase B (PKB), is arguably the most important signalling nexus in the cell. Akt integrates a plethora of extracellular signals to generate diverse outcomes, including proliferation, motility, ...

    Abstract The protein serine/threonine kinase Akt, also known as protein kinase B (PKB), is arguably the most important signalling nexus in the cell. Akt integrates a plethora of extracellular signals to generate diverse outcomes, including proliferation, motility, growth, glucose homeostasis, survival, and cell death. The phosphatidylinositol 3-kinase (PI3K)/Akt pathway is the second most frequently mutated pathway in cancer, after p53, and mutations in components of this pathway are found in around 70% of breast cancers. Thus, understanding how Akt relays input signals to downstream effectors is critically important for the design of therapeutic strategies to combat breast cancer. In this review, we will discuss the various signals upstream of Akt that impact on its activity, how Akt integrates these signals and modulates the activity of downstream targets to control mammary gland development, and how mutations in components of the pathway result in breast cancer.
    Mesh-Begriff(e) Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Epithelium/metabolism ; Female ; Humans ; Mammary Glands, Human/metabolism ; Models, Biological ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction
    Chemische Substanzen Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; AKT1 protein, human (EC 2.7.11.1) ; AKT2 protein, human (EC 2.7.11.1) ; AKT3 protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2010-04-09
    Erscheinungsland England
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2015059-3
    ISSN 1465-542X ; 1465-5411
    ISSN (online) 1465-542X
    ISSN 1465-5411
    DOI 10.1186/bcr2558
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: A community developed conceptual model for reducing long-term health problems in children with intellectual disability in India.

    Nair, Manisha / Hazarika, Mythili / Kishore, M Thomas / Sengupta, Nabarun / Sheregar, Ganesh / MacGregor, Hayley / Wickenden, Mary / Kaushik, Neel Harit / Saikia, Prarthana / Kelley, Maureen / Shepperd, Sasha

    PLOS global public health

    2023  Band 3, Heft 4, Seite(n) e0000833

    Abstract: ... communicable diseases among children with ID in India. From April through to July 2020 we undertook community engagement ...

    Abstract Children with intellectual disability (ID) have a higher risk of long-term health problems in adulthood. India has the highest prevalence of ID of any country with 1.6 million under-five children living with the condition. Despite this, compared with other children, this neglected population is excluded from mainstream disease prevention and health promotion programmes. Our objective was to develop an evidence-based conceptual framework for a needs-based inclusive intervention to reduce the risk of communicable and non-communicable diseases among children with ID in India. From April through to July 2020 we undertook community engagement and involvement activities in ten States in India using a community-based participatory approach, guided by the bio-psycho-social model. We adapted the five steps recommended for the design and evaluation of a public participation process for the health sector. Seventy stakeholders from ten States contributed to the project: 44 parents and 26 professionals who work with people with ID. We mapped the outputs from two rounds of stakeholder consultations with evidence from systematic reviews to develop a conceptual framework that underpins an approach to develop a cross-sectoral family-centred needs-based inclusive intervention to improve health outcomes for children with ID. A working Theory of Change model delineates a pathway that reflected the priorities of the target population. We discussed the models during a third round of consultations to identify limitations, relevance of the concepts, structural and social barriers that could influence acceptability and adherence, success criteria, and integration with existing health system and service delivery. There are currently no health promotion programmes focusing on children with ID in India despite the population being at a higher risk of developing comorbid health problems. Therefore, an urgent next step is to test the conceptual model to determine acceptance and effectiveness within the context of socio-economic challenges faced by the children and their families in the country.
    Sprache Englisch
    Erscheinungsdatum 2023-04-14
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 2767-3375
    ISSN (online) 2767-3375
    DOI 10.1371/journal.pgph.0000833
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  3. Artikel ; Online: Conditional deletion of Stat3 in mammary epithelium impairs the acute phase response and modulates immune cell numbers during post-lactational regression.

    Hughes, Katherine / Wickenden, Julie A / Allen, Judith E / Watson, Christine J

    The Journal of pathology

    2012  Band 227, Heft 1, Seite(n) 106–117

    Abstract: Mammary gland regression following weaning (involution) is associated with extensive cell death and the acquisition of an inflammatory signature. Characterizing the interplay between mammary epithelial cells, the re-emerging stroma and immune cells has ... ...

    Abstract Mammary gland regression following weaning (involution) is associated with extensive cell death and the acquisition of an inflammatory signature. Characterizing the interplay between mammary epithelial cells, the re-emerging stroma and immune cells has implications for the understanding of the pathogenesis of pregnancy-associated breast cancer. Stat3 has a role in orchestrating cell death and involution, and we sought to determine whether expression of Stat3 by the mammary epithelium also influences the innate immune environment and inflammatory cell influx in the gland. We examined mice in which Stat3 is conditionally deleted only in the mammary epithelium. Distinct sets of genes associated with the acute phase response and innate immunity are markedly up-regulated during first phase involution in a Stat3-dependent manner. During second phase involution, chitinase 3-like 1, which has been associated with wound healing and chronic inflammatory conditions, is dramatically up-regulated by Stat3. Also at this time, the number of mammary macrophages and mast cells increases per unit area, and this increase is impaired in the absence of epithelial Stat3. Furthermore, expression of arginase-1 and Ym1, markers of alternatively activated macrophages, is significantly decreased in the absence of Stat3, whilst iNOS, a marker associated with classically activated macrophages, shows significantly increased expression in the Stat3-deleted glands. Thus, Stat3 is a key transcriptional regulator of genes associated with innate immunity and wound healing and influences mammary macrophage and mast cell numbers. The presence of epithelial Stat3 appears to polarize the macrophages and epithelial cells towards an alternatively activated phenotype, since in the absence of Stat3, the gland retains a phenotype associated with classically activated macrophages. These findings have relevance to the study of pregnancy-associated breast cancer and the role of Stat3 signalling in recruitment of alternatively activated tumour-associated macrophages in breast cancer.
    Mesh-Begriff(e) Acute-Phase Reaction/genetics ; Acute-Phase Reaction/immunology ; Acute-Phase Reaction/metabolism ; Animals ; Cell Count ; Cell Death ; Cell Line ; Epithelial Cells/cytology ; Epithelial Cells/immunology ; Epithelial Cells/metabolism ; Female ; Gene Deletion ; Immunity, Innate/genetics ; Immunity, Innate/immunology ; Lactation/physiology ; Macrophage Activation/genetics ; Macrophage Activation/immunology ; Macrophages/cytology ; Macrophages/metabolism ; Mammary Glands, Animal/cytology ; Mammary Glands, Animal/immunology ; Mammary Glands, Animal/metabolism ; Mast Cells/cytology ; Mast Cells/metabolism ; Mice ; Mice, Knockout ; STAT3 Transcription Factor/deficiency ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism ; Up-Regulation ; Weaning ; Wound Healing/genetics ; Wound Healing/immunology
    Chemische Substanzen STAT3 Transcription Factor ; Stat3 protein, mouse
    Sprache Englisch
    Erscheinungsdatum 2012-01-27
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3119-7
    ISSN 1096-9896 ; 0022-3417
    ISSN (online) 1096-9896
    ISSN 0022-3417
    DOI 10.1002/path.3961
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Differential reprogramming of isogenic colorectal cancer cells by distinct activating KRAS mutations.

    Hammond, Dean E / Mageean, Craig J / Rusilowicz, Emma V / Wickenden, Julie A / Clague, Michael J / Prior, Ian A

    Journal of proteome research

    2015  Band 14, Heft 3, Seite(n) 1535–1546

    Abstract: Oncogenic mutations of Ras at codons 12, 13, or 61, that render the protein constitutively active, are found in ∼ 16% of all cancer cases. Among the three major Ras isoforms, KRAS is the most frequently mutated isoform in cancer. Each Ras isoform and ... ...

    Abstract Oncogenic mutations of Ras at codons 12, 13, or 61, that render the protein constitutively active, are found in ∼ 16% of all cancer cases. Among the three major Ras isoforms, KRAS is the most frequently mutated isoform in cancer. Each Ras isoform and tumor type displays a distinct pattern of codon-specific mutations. In colon cancer, KRAS is typically mutated at codon 12, but a significant fraction of patients have mutations at codon 13. Clinical data suggest different outcomes and responsiveness to treatment between these two groups. To investigate the differential effects upon cell status associated with KRAS mutations we performed a quantitative analysis of the proteome and phosphoproteome of isogenic SW48 colon cancer cell lines in which one allele of the endogenous gene has been edited to harbor specific KRAS mutations (G12V, G12D, or G13D). Each mutation generates a distinct signature, with the most variability seen between G13D and the codon 12 KRAS mutants. One notable example of specific up-regulation in KRAS codon 12 mutant SW48 cells is provided by the short form of the colon cancer stem cell marker doublecortin-like Kinase 1 (DCLK1) that can be reversed by suppression of KRAS.
    Mesh-Begriff(e) Cell Line, Tumor ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Genes, ras ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Mutation ; Protein-Serine-Threonine Kinases/metabolism ; Proteomics ; Up-Regulation
    Chemische Substanzen Intracellular Signaling Peptides and Proteins ; DCLK1 protein, human (EC 2.7.1.11) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2015-03-06
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2078618-9
    ISSN 1535-3907 ; 1535-3893
    ISSN (online) 1535-3907
    ISSN 1535-3893
    DOI 10.1021/pr501191a
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: A community developed conceptual model for reducing long-term health problems in children with intellectual disability in India.

    Manisha Nair / Mythili Hazarika / M Thomas Kishore / Nabarun Sengupta / Ganesh Sheregar / Hayley MacGregor / Mary Wickenden / Neel Harit Kaushik / Prarthana Saikia / Maureen Kelley / Sasha Shepperd

    PLOS Global Public Health, Vol 3, Iss 4, p e

    2023  Band 0000833

    Abstract: ... communicable diseases among children with ID in India. From April through to July 2020 we undertook community engagement ...

    Abstract Children with intellectual disability (ID) have a higher risk of long-term health problems in adulthood. India has the highest prevalence of ID of any country with 1.6 million under-five children living with the condition. Despite this, compared with other children, this neglected population is excluded from mainstream disease prevention and health promotion programmes. Our objective was to develop an evidence-based conceptual framework for a needs-based inclusive intervention to reduce the risk of communicable and non-communicable diseases among children with ID in India. From April through to July 2020 we undertook community engagement and involvement activities in ten States in India using a community-based participatory approach, guided by the bio-psycho-social model. We adapted the five steps recommended for the design and evaluation of a public participation process for the health sector. Seventy stakeholders from ten States contributed to the project: 44 parents and 26 professionals who work with people with ID. We mapped the outputs from two rounds of stakeholder consultations with evidence from systematic reviews to develop a conceptual framework that underpins an approach to develop a cross-sectoral family-centred needs-based inclusive intervention to improve health outcomes for children with ID. A working Theory of Change model delineates a pathway that reflected the priorities of the target population. We discussed the models during a third round of consultations to identify limitations, relevance of the concepts, structural and social barriers that could influence acceptability and adherence, success criteria, and integration with existing health system and service delivery. There are currently no health promotion programmes focusing on children with ID in India despite the population being at a higher risk of developing comorbid health problems. Therefore, an urgent next step is to test the conceptual model to determine acceptance and effectiveness within the context of socio-economic challenges ...
    Schlagwörter Public aspects of medicine ; RA1-1270
    Thema/Rubrik (Code) 360
    Sprache Englisch
    Erscheinungsdatum 2023-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel: Differential Reprogramming of Isogenic Colorectal Cancer Cells by Distinct Activating KRAS Mutations

    Hammond, Dean E / Mageean, Craig J / Rusilowicz, Emma V / Wickenden, Julie.A / Clague, Michael J / Prior, Ian A

    Journal of Proteome Research. 2015 Mar. 06, v. 14, no. 3

    2015  

    Abstract: Oncogenic mutations of Ras at codons 12, 13, or 61, that render the protein constitutively active, are found in ∼16% of all cancer cases. Among the three major Ras isoforms, KRAS is the most frequently mutated isoform in cancer. Each Ras isoform and ... ...

    Abstract Oncogenic mutations of Ras at codons 12, 13, or 61, that render the protein constitutively active, are found in ∼16% of all cancer cases. Among the three major Ras isoforms, KRAS is the most frequently mutated isoform in cancer. Each Ras isoform and tumor type displays a distinct pattern of codon-specific mutations. In colon cancer, KRAS is typically mutated at codon 12, but a significant fraction of patients have mutations at codon 13. Clinical data suggest different outcomes and responsiveness to treatment between these two groups. To investigate the differential effects upon cell status associated with KRAS mutations we performed a quantitative analysis of the proteome and phosphoproteome of isogenic SW48 colon cancer cell lines in which one allele of the endogenous gene has been edited to harbor specific KRAS mutations (G12V, G12D, or G13D). Each mutation generates a distinct signature, with the most variability seen between G13D and the codon 12 KRAS mutants. One notable example of specific up-regulation in KRAS codon 12 mutant SW48 cells is provided by the short form of the colon cancer stem cell marker doublecortin-like Kinase 1 (DCLK1) that can be reversed by suppression of KRAS.
    Schlagwörter alleles ; cell lines ; codons ; colorectal neoplasms ; mutants ; mutation ; neoplasm cells ; patients ; proteome ; quantitative analysis ; stem cells
    Sprache Englisch
    Erscheinungsverlauf 2015-0306
    Umfang p. 1535-1546.
    Erscheinungsort American Chemical Society
    Dokumenttyp Artikel
    ZDB-ID 2078618-9
    ISSN 1535-3907 ; 1535-3893
    ISSN (online) 1535-3907
    ISSN 1535-3893
    DOI 10.1021%2Fpr501191a
    Datenquelle NAL Katalog (AGRICOLA)

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  7. Artikel: Cigarette smoke prevents apoptosis through inhibition of caspase activation and induces necrosis.

    Wickenden, Julie A / Clarke, Murray C H / Rossi, Adriano G / Rahman, Irfan / Faux, Stephen P / Donaldson, Kenneth / MacNee, William

    American journal of respiratory cell and molecular biology

    2003  Band 29, Heft 5, Seite(n) 562–570

    Abstract: Emphysema is characterized by enlargement of the distal airspaces in the lungs due to destruction of alveolar walls. Alveolar endothelial and epithelial cell apoptosis induced by cigarette smoke is thought to be a possible mechanism for this cell loss. ... ...

    Abstract Emphysema is characterized by enlargement of the distal airspaces in the lungs due to destruction of alveolar walls. Alveolar endothelial and epithelial cell apoptosis induced by cigarette smoke is thought to be a possible mechanism for this cell loss. In contrast, our studies show that cigarette smoke condensate (CSC) induces necrosis in alveolar epithelial cells and human umbilical vein endothelial cells. Furthermore, study of the cell death pathway in a model system using Jurkat cells revealed that in addition to inducing necrosis, CSC inhibited apoptosis induced by staurosporine or Fas ligation, with both effects prevented by the antioxidants glutathione and dithiothreitol. Time course experiments revealed that CSC inhibited an early step in the caspase cascade, whereby caspase-3 was not activated. Moreover, cell-free reconstitution of the apoptosome in cytoplasmic extracts from CSC-treated cells, by addition of cytochrome-c and dATP, did not result in activation of caspases-3 or -9. Thus, smoke treatment may alter the levels of pro- and antiapoptogenic factors downstream of the mitochondria to inhibit active apoptosome formation. Therefore, unlike previous studies, cell death in response to cigarette smoke by necrosis and not apoptosis may be responsible for the loss of alveolar walls and inflammation observed in emphysema.
    Mesh-Begriff(e) Apoptosis/physiology ; Caspases/metabolism ; Endothelium, Vascular/pathology ; Endothelium, Vascular/physiology ; Enzyme Activation/physiology ; Epithelium/pathology ; Epithelium/physiology ; Humans ; Jurkat Cells ; Necrosis ; Pulmonary Alveoli/pathology ; Pulmonary Alveoli/physiology ; Smoking/metabolism
    Chemische Substanzen Caspases (EC 3.4.22.-)
    Sprache Englisch
    Erscheinungsdatum 2003-11
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2002-0235OC
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel: ERK1/2-dependent phosphorylation of BimEL promotes its rapid dissociation from Mcl-1 and Bcl-xL.

    Ewings, Katherine E / Hadfield-Moorhouse, Kathryn / Wiggins, Ceri M / Wickenden, Julie A / Balmanno, Kathryn / Gilley, Rebecca / Degenhardt, Kurt / White, Eileen / Cook, Simon J

    The EMBO journal

    2007  Band 26, Heft 12, Seite(n) 2856–2867

    Abstract: The proapoptotic protein Bim is expressed de novo following withdrawal of serum survival factors. Here, we show that Bim-/- fibroblasts and epithelial cells exhibit reduced cell death following serum withdrawal in comparison with their wild-type ... ...

    Abstract The proapoptotic protein Bim is expressed de novo following withdrawal of serum survival factors. Here, we show that Bim-/- fibroblasts and epithelial cells exhibit reduced cell death following serum withdrawal in comparison with their wild-type counterparts. In viable cells, Bax associates with Bcl-2, Bcl-x(L) and Mcl-1. Upon serum withdrawal, newly expressed Bim(EL) associates with Bcl-x(L) and Mcl-1, coinciding with the dissociation of Bax from these proteins. Survival factors can prevent association of Bim with pro-survival proteins by preventing Bim expression. However, we now show that even preformed Bim(EL)/Mcl-1 and Bim(EL)/Bcl-x(L) complexes can be rapidly dissociated following activation of ERK1/2 by survival factors. The dissociation of Bim from Mcl-1 is specific for Bim(EL) and requires ERK1/2-dependent phosphorylation of Bim(EL) at Ser(65). Finally, ERK1/2-dependent dissociation of Bim(EL) from Mcl-1 and Bcl-x(L) may play a role in regulating Bim(EL) degradation, since mutations in the Bim(EL) BH3 domain that disrupt binding to Mcl-1 cause increased turnover of Bim(EL). These results provide new insights into the role of Bim in cell death and its regulation by the ERK1/2 survival pathway.
    Mesh-Begriff(e) Apoptosis Regulatory Proteins/metabolism ; Bcl-2-Like Protein 11 ; Cell Line ; Culture Media, Serum-Free ; Humans ; Membrane Proteins/metabolism ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasm Proteins/metabolism ; Phosphorylation ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; bcl-X Protein/metabolism
    Chemische Substanzen Apoptosis Regulatory Proteins ; BCL2L11 protein, human ; Bcl-2-Like Protein 11 ; Culture Media, Serum-Free ; Membrane Proteins ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasm Proteins ; Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-bcl-2 ; bcl-X Protein ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24)
    Sprache Englisch
    Erscheinungsdatum 2007-05-24
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 586044-1
    ISSN 1460-2075 ; 0261-4189
    ISSN (online) 1460-2075
    ISSN 0261-4189
    DOI 10.1038/sj.emboj.7601723
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Buch ; Online: ERK1/2-dependent phosphorylation of BimEL promotes its rapid dissociation from Mcl-1 and Bcl-xL

    Ewings, Katherine E / Balmanno, Kathryn / Wickenden, Julie A / Cook, Simon J / Degenhardt, Kurt / Wiggins, Ceri M / Hadfield-Moorhouse, Kathryn / Gilley, Rebecca / White, Eileen

    2007  

    Abstract: Research Support, Non-U.S. Gov't ... Journal Article ... The proapoptotic protein Bim is expressed de novo following withdrawal of serum survival factors. Here, we show that Bim-/- fibroblasts and epithelial cells exhibit reduced cell death following serum ... ...

    Abstract Research Support, Non-U.S. Gov't

    Journal Article

    The proapoptotic protein Bim is expressed de novo following withdrawal of serum survival factors. Here, we show that Bim-/- fibroblasts and epithelial cells exhibit reduced cell death following serum withdrawal in comparison with their wild-type counterparts. In viable cells, Bax associates with Bcl-2, Bcl-x(L) and Mcl-1. Upon serum withdrawal, newly expressed Bim(EL) associates with Bcl-x(L) and Mcl-1, coinciding with the dissociation of Bax from these proteins. Survival factors can prevent association of Bim with pro-survival proteins by preventing Bim expression. However, we now show that even preformed Bim(EL)/Mcl-1 and Bim(EL)/Bcl-x(L) complexes can be rapidly dissociated following activation of ERK1/2 by survival factors. The dissociation of Bim from Mcl-1 is specific for Bim(EL) and requires ERK1/2-dependent phosphorylation of Bim(EL) at Ser(65). Finally, ERK1/2-dependent dissociation of Bim(EL) from Mcl-1 and Bcl-x(L) may play a role in regulating Bim(EL) degradation, since mutations in the Bim(EL) BH3 domain that disrupt binding to Mcl-1 cause increased turnover of Bim(EL). These results provide new insights into the role of Bim in cell death and its regulation by the ERK1/2 survival pathway.
    Sprache Englisch
    Erscheinungsdatum 2007-05-24
    Dokumenttyp Buch ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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