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Charlotte Church

Welsh singer and songwriter (born 1986)

Charlotte Church

Church performing at the FOCUS Wales Festival in 2013

Born

Charlotte Maria Reed


(1986-02-21) 21 February 1986 (age 39)

Cardiff, Wales

Occupations
  • Singer
  • songwriter
  • actress
  • presenter
Years active1997–present
Spouse

Jonathan Powell

(m. 2017)​
Children3
Musical career
Genres
InstrumentVocals
LabelsSony
Power Amp

Musical artist

Charlotte Maria Church (born Charlotte Maria Reed, 21 February 1986) is a Welsh singer-songwriter, actress, and television presenter from Cardiff.

As a child, Church was a popular classical singer with a less-successful attempt to move into pop music in 2005. By 2007, she had sold more than ten million records worldwide including over five million in the United States. She hosted a Channel 4 chat show titled The Charlotte Church Show. Church released her first album in five years, titled Back to Scratch, on 25 October 2010. Church is a soprano.

In recent years, Church has embraced political activism, supporting Jeremy Corbyn when he led the Labour party, Plaid Cymru in the Senedd elections, and the cause of Welsh independence.

Early life

Church was born Charlotte Maria Reed in Llandaff, a district of Cardiff, Wales, to Maria and computer engineer Stephen Reed. Her parents separated when she was two, and she was raised by her mother who brought her up as a Roman Catholic. In 1992, Maria married her second husband, James Church, who adopted Charlotte in 1999. She has four siblings: two younger half-brothers, through her biological father, and two older step-siblings from her adoptive father's previous marriage.

Charlotte's musical break came at age 11 when she sang Andrew Lloyd Webber's "Pie Jesu" over the telephone on the televisi

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  • Member Biography

    I am an immunologist with a strong expertise in adaptive immune responses to cancer. Challenging the view that chemotherapies only mediate their anticancer activity through a direct cytotoxic activity on tumor cells, my Ph.D. work uncovered a critical contribution of anticancer immune responses for the success of conventional therapies. This work prompted the design of novel strategies enhancing the efficacy of anticancer therapies by manipulating the immune system. During my postdoctoral work at Harvard University, I underscored the relevance of concomitant Tim-3 and PD-1 blockade to prevent T cell dysfunction and restore anticancer immunity. After returning to France, I set up my laboratory and showed the anticancer properties of a novel subset of CD4 T cells, IL-9-producing TH9 cells, upon adoptive transfer against melanoma. Thanks to funding from the European Commission, I developed in my laboratory multiple models of combination treatments with chemotherapy and immunomodulation to interrogate the relevance of T cells in anticancer cancer immune responses. In January 2023, I joined the Brown Center for Immunotherapy (Indianapolis, IN) as Christopher Brown Professor of Immunology to pursue the discovery of novel molecular targets that can be therapeutically exploited to enhance T cell functions. For this, my laboratory will combine in vitro and in vivo approaches including advanced gene and protein expression analysis of mouse and human T cells, immunological investigation of the anticancer responses in transgenic, gene-deficient mice as well as spontaneous and transplantable models of cancers.

    Post-doctoral Fellowship - Harvard Medical School, Boston, MA2010

    Ph.D. - University of Paris-Saclay2008

    The Autophagy Lysosomal Pathway and Neurodegeneration

    Abstract

    The autophagy lysosomal pathway (ALP) is a major mechanism for degrading intracellular macromolecules. The catabolic products can then be used by the cell for energy or as building blocks to make other macromolecules. Since its discovery, a variety of cellular pathways have emerged that target components with varying specificity for lysosomal degradation. Under some circumstances, lysosomes may release their contents into the extracellular space where they may serve signaling or pathogenic functions. The ALP is active in healthy cells, and the level of activity can be regulated by nutrient-sensing and metabolic signaling pathways. The ALP is the primary pathway by which lipids and damaged organelles are degraded and may be the only pathway capable of degrading aggregated proteins. As such, there has been intense interest in understanding the role of the ALP in the accumulation of aggregated misfolded proteins characteristic of many of the major adult-onset neurodegenerative diseases. This review focuses on recent advances in our understanding of the ALP and its potential relationship to the pathogenesis and treatment of neurodegenerative diseases.

    HISTORY

    The work of Drs. Christian de Duve and Yoshinori Ohsumi led to the discovery of the autophagy lysosomal pathway (ALP), and the contributions of each were recognized with the awards of the Nobel prize in physiology or medicine in 1974 and 2016, respectively. de Duve discovered the membrane-bound acidic compartment called the lysosome with biochemistry approaches (De Duve and Wattiaux 1966). Ohsumi discovered the core machinery responsible for autophagy by identifying the genes in yeast that are necessary for survival in the setting of caloric restriction (Klionsky et al. 2003; Tooze and Dikic 2016).

    LYSOSOME—THE HUB OF A PROTEOSTASIS NETWORK

    The common way to portray the ALP is as a unidirectional pathway that begins with the de novo formation o

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