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  1. Book ; Online ; Thesis: Just Lunch: An Ethnography of School Meals and Poverty in Delhi

    Bonaker, Alva [Verfasser] / Roy, Srirupa [Akademischer Betreuer] / Roy, Srirupa [Gutachter] / Viswanath, Rupa [Gutachter] / Balagopalan, Sarada [Gutachter]

    2023  

    Author's details Alva Bonaker ; Gutachter: Srirupa Roy, Rupa Viswanath, Sarada Balagopalan ; Betreuer: Srirupa Roy
    Keywords Sozialwissenschaften, Soziologie ; Social Sciences, Sociology
    Subject code sg300
    Language English
    Publisher Niedersächsische Staats- und Universitätsbibliothek Göttingen
    Publishing place Göttingen
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  2. Book ; Online ; Thesis: City on the Move: Migration, Public Culture, and Urban Identity in Delhi, c. 1911-present

    Ahmad, Saeed [Verfasser] / Roy, Srirupa [Akademischer Betreuer] / Kaur, Ravinder [Gutachter] / Viswanath, Rupa [Gutachter]

    2023  

    Author's details Saeed Ahmad ; Gutachter: Ravinder Kaur, Rupa Viswanath ; Betreuer: Srirupa Roy
    Keywords Sozialwissenschaften, Soziologie ; Social Sciences, Sociology
    Subject code sg300
    Language English
    Publisher Niedersächsische Staats- und Universitätsbibliothek Göttingen
    Publishing place Göttingen
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  3. Article ; Online: Autophagy enables retromer-dependent plasma membrane translocation of SLC2A1/GLUT1 to enhance glucose uptake.

    Roy, Srirupa / Debnath, Jayanta

    Autophagy

    2017  Volume 13, Issue 11, Page(s) 2013–2014

    MeSH term(s) Autophagy ; Biological Transport ; Cell Membrane ; Glucose
    Chemical Substances Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2017-09-28
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2017.1371397
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6741: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  4. Book ; Conference proceedings: Visualizing secularism and religion

    Çınar, Alev / Roy, Srirupa / Yahya, Maha

    Egypt, Lebanon, Turkey, India ; [... public spheres workshop that took place at Bilkent Üniversitesi, Ankara, Turkey on October 15 - 17, 2004]

    2012  

    Institution Bilkent Üniversitesi
    Event/congress Public spheres workshop (2004.10.15-17, Ankara)
    Author's details Alev Çınar; Srirupa Roy, and Maha Yahya, ed
    Keywords Religion ; Religion and politics ; Secularism
    Language English
    Size 348 S., Ill., Kt.
    Publisher Univ. of Michigan Press
    Publishing place Ann Arbor, Mich
    Document type Book ; Conference proceedings
    Note Includes bibliographical references and index
    ISBN 0472071181 ; 9780472071180
    Database Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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  5. Book ; Conference proceedings: Visualizing secularism and religion

    Çınar, Alev / Roy, Srirupa / Yahya, Maha

    Egypt, Lebanon, Turkey, India ; [... public spheres workshop that took place at Bilkent Üniversitesi, Ankara, Turkey on October 15 - 17, 2004]

    2012  

    Institution Bilkent Üniversitesi
    Event/congress Public spheres workshop (2004.10.15-17, Ankara)
    Author's details Alev Çınar; Srirupa Roy, and Maha Yahya, ed
    Keywords Religion ; Religion and politics ; Secularism
    Language English
    Size 348 S., Ill., Kt.
    Publisher Univ. of Michigan Press
    Publishing place Ann Arbor, Mich
    Document type Book ; Conference proceedings
    Note Includes bibliographical references and index
    ISBN 0472071181 ; 9780472071180
    Database Former special subject collection: coastal and deep sea fishing

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  6. Article ; Online: Autophagy in stromal fibroblasts promotes tumor desmoplasia and mammary tumorigenesis.

    Rudnick, Jenny A / Monkkonen, Teresa / Mar, Florie A / Barnes, James M / Starobinets, Hanna / Goldsmith, Juliet / Roy, Srirupa / Bustamante Eguiguren, Sofía / Weaver, Valerie M / Debnath, Jayanta

    Genes & development

    2021  Volume 35, Issue 13-14, Page(s) 963–975

    Abstract: Autophagy inhibitors are currently being evaluated in clinical trials for the treatment of diverse cancers, largely due to their ability to impede tumor cell survival and metabolic adaptation. More recently, there is growing interest in whether and how ... ...

    Abstract Autophagy inhibitors are currently being evaluated in clinical trials for the treatment of diverse cancers, largely due to their ability to impede tumor cell survival and metabolic adaptation. More recently, there is growing interest in whether and how modulating autophagy in the host stroma influences tumorigenesis. Fibroblasts play prominent roles in cancer initiation and progression, including depositing type 1 collagen and other extracellular matrix (ECM) components, thereby stiffening the surrounding tissue to enhance tumor cell proliferation and survival, as well as secreting cytokines that modulate angiogenesis and the immune microenvironment. This constellation of phenotypes, pathologically termed desmoplasia, heralds poor prognosis and reduces patient survival. Using mouse mammary cancer models and syngeneic transplantation assays, we demonstrate that genetic ablation of stromal fibroblast autophagy significantly impedes fundamental elements of the stromal desmoplastic response, including collagen and proinflammatory cytokine secretion, extracellular matrix stiffening, and neoangiogenesis. As a result, autophagy in stromal fibroblasts is required for mammary tumor growth in vivo, even when the cancer cells themselves remain autophagy-competent . We propose the efficacy of autophagy inhibition is shaped by this ability of host stromal fibroblast autophagy to support tumor desmoplasia.
    MeSH term(s) Animals ; Autophagy/genetics ; Cell Line, Tumor ; Cell Transformation, Neoplastic/pathology ; Fibroblasts/metabolism ; Humans ; Mice ; Stromal Cells ; Tumor Microenvironment/genetics
    Language English
    Publishing date 2021-06-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 806684-x
    ISSN 1549-5477 ; 0890-9369
    ISSN (online) 1549-5477
    ISSN 0890-9369
    DOI 10.1101/gad.345629.120
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2292: Show issues Location:
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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
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    Zs.MG 54: Show issues

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  7. Article ; Online: Autophagy and tumorigenesis.

    Roy, Srirupa / Debnath, Jayanta

    Seminars in immunopathology

    2010  Volume 32, Issue 4, Page(s) 383–396

    Abstract: Autophagy, a catabolic process involved in the sequestration and lysosomal degradation of cytoplasmic contents, is crucial for cellular homeostasis. The current literature supports that autophagy plays diverse roles in the development, maintenance, and ... ...

    Abstract Autophagy, a catabolic process involved in the sequestration and lysosomal degradation of cytoplasmic contents, is crucial for cellular homeostasis. The current literature supports that autophagy plays diverse roles in the development, maintenance, and progression of tumors. While genetic evidence indicates autophagy functions as a tumor suppressor mechanism, it is also apparent that autophagy can promote the survival of established tumors under stress conditions and in response to chemotherapy. In this review, we discuss the mechanisms and the evidence underlying these multifaceted roles of autophagy in tumorigenesis, the prospects for targeting autophagy in cancer therapy, and overview the potential markers that may be utilized to reliably detect autophagy in clinical settings.
    MeSH term(s) Animals ; Autophagy/immunology ; Biomarkers, Tumor/immunology ; Cell Survival/immunology ; Humans ; Lysosomes/immunology ; Neoplasms/immunology ; Neoplasms/pathology ; Neoplasms/therapy
    Chemical Substances Biomarkers, Tumor
    Language English
    Publishing date 2010-06-30
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2316828-6
    ISSN 1863-2300 ; 1863-2297
    ISSN (online) 1863-2300
    ISSN 1863-2297
    DOI 10.1007/s00281-010-0213-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1425: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  8. Article: Autophagy-Dependent Shuttling of TBC1D5 Controls Plasma Membrane Translocation of GLUT1 and Glucose Uptake

    Roy, Srirupa / Andrew M. Leidal / Jayanta Debnath / Jordan Ye / Sabrina M. Ronen

    Molecular cell. 2017 July 06, v. 67, no. 1

    2017  

    Abstract: Autophagy traditionally sustains metabolism in stressed cells by promoting intracellular catabolism and nutrient recycling. Here, we demonstrate that in response to stresses requiring increased glycolytic demand, the core autophagy machinery also ... ...

    Abstract Autophagy traditionally sustains metabolism in stressed cells by promoting intracellular catabolism and nutrient recycling. Here, we demonstrate that in response to stresses requiring increased glycolytic demand, the core autophagy machinery also facilitates glucose uptake and glycolytic flux by promoting cell surface expression of the glucose transporter GLUT1/Slc2a1. During metabolic stress, LC3+ autophagic compartments bind and sequester the RabGAP protein TBC1D5 away from its inhibitory interactions with the retromer complex, thereby enabling retromer recruitment to endosome membranes and GLUT1 plasma membrane translocation. In contrast, TBC1D5 inhibitory interactions with the retromer are maintained in autophagy-deficient cells, leading to GLUT1 mis-sorting into endolysosomal compartments. Furthermore, TBC1D5 depletion in autophagy-deficient cells rescues retromer recruitment to endosomal membranes and GLUT1 surface recycling. Hence, TBC1D5 shuttling to autophagosomes during metabolic stress facilitates retromer-dependent GLUT1 trafficking. Overall, our results illuminate key interconnections between the autophagy and endosomal pathways dictating GLUT1 trafficking and extracellular nutrient uptake.
    Keywords autophagy ; biogeochemical cycles ; glucose ; glucose transporters ; glycolysis ; nutrient uptake ; plasma membrane
    Language English
    Dates of publication 2017-0706
    Size p. 84-95.e5.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2017.05.020
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

    Z 2005/501: Show issues

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  9. Article ; Online: Autophagy-Dependent Shuttling of TBC1D5 Controls Plasma Membrane Translocation of GLUT1 and Glucose Uptake.

    Roy, Srirupa / Leidal, Andrew M / Ye, Jordan / Ronen, Sabrina M / Debnath, Jayanta

    Molecular cell

    2017  Volume 67, Issue 1, Page(s) 84–95.e5

    Abstract: Autophagy traditionally sustains metabolism in stressed cells by promoting intracellular catabolism and nutrient recycling. Here, we demonstrate that in response to stresses requiring increased glycolytic demand, the core autophagy machinery also ... ...

    Abstract Autophagy traditionally sustains metabolism in stressed cells by promoting intracellular catabolism and nutrient recycling. Here, we demonstrate that in response to stresses requiring increased glycolytic demand, the core autophagy machinery also facilitates glucose uptake and glycolytic flux by promoting cell surface expression of the glucose transporter GLUT1/Slc2a1. During metabolic stress, LC3
    MeSH term(s) Animals ; Autophagosomes/metabolism ; Autophagosomes/pathology ; Autophagy ; Autophagy-Related Protein 5/genetics ; Autophagy-Related Protein 5/metabolism ; Autophagy-Related Protein 7/genetics ; Autophagy-Related Protein 7/metabolism ; Cell Membrane/metabolism ; Endosomes/metabolism ; Endosomes/pathology ; Female ; Fibroblasts/metabolism ; Fibroblasts/pathology ; GTPase-Activating Proteins/genetics ; GTPase-Activating Proteins/metabolism ; Glucose/metabolism ; Glucose Transporter Type 1/genetics ; Glucose Transporter Type 1/metabolism ; Glycolysis ; HEK293 Cells ; Humans ; Kinetics ; Lysosomes/metabolism ; Lysosomes/pathology ; Mice ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Protein Transport ; RNA Interference ; Signal Transduction ; Stress, Physiological ; Transfection ; Vesicular Transport Proteins/genetics ; Vesicular Transport Proteins/metabolism
    Chemical Substances Atg5 protein, mouse ; Atg7 protein, mouse ; Autophagy-Related Protein 5 ; GTPase-Activating Proteins ; Glucose Transporter Type 1 ; Map1lc3b protein, mouse ; Microtubule-Associated Proteins ; SLC2A1 protein, human ; Slc2a1 protein, mouse ; TBC1D5 protein, human ; Tbc1d5 protein, mouse ; Vesicular Transport Proteins ; Vps35 protein, mouse ; Autophagy-Related Protein 7 (EC 6.2.1.45) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2017-06-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2017.05.020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5055: 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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  10. Article ; Online: Silibinin prevents ultraviolet B radiation-induced epidermal damages in JB6 cells and mouse skin in a p53-GADD45α-dependent manner.

    Roy, Srirupa / Deep, Gagan / Agarwal, Chapla / Agarwal, Rajesh

    Carcinogenesis

    2011  Volume 33, Issue 3, Page(s) 629–636

    Abstract: Better preventive strategies are required to reduce ultraviolet (UV)-caused photodamage, the primary etiological factor for non-melanoma skin cancer (NMSC). Accordingly, here we examined the preventive efficacy of silibinin against UVB-induced ... ...

    Abstract Better preventive strategies are required to reduce ultraviolet (UV)-caused photodamage, the primary etiological factor for non-melanoma skin cancer (NMSC). Accordingly, here we examined the preventive efficacy of silibinin against UVB-induced photodamage using mouse epidermal JB6 cells and SKH1 hairless mouse epidermis. In JB6 cells, silibinin pretreatment protected against apoptosis and accelerated the repair of cyclobutane pyrimidine dimers (CPD) induced by moderate dose of UVB (50 mJ/cm(2)), which we are at risk of daily exposure. Silibinin also reversed UVB-induced S phase arrest, reducing both active DNA synthesizing and inactive S phase populations. In mechanistic studies, UVB-irradiated cells showed a transient upregulation of both phosphorylated (Ser-15 and Ser-392) and total p53, whereas silibinin pretreatment led to a more sustained upregulation and stronger nuclear localization of p53. Silibinin also caused a marked upregulation of GADD45α, a downstream target of p53, implicated in DNA repair and cell cycle regulation. Importantly, under p53 and GADD45α knockdown conditions, cells were more susceptible to UVB-induced apoptosis without any significant S phase arrest, and protective effects of silibinin were compromised. Similar to the in vitro results, topical application of silibinin prior to or immediately after UVB irradiation resulted in sustained increase in p53 and GADD45α levels and accelerated CPD removal in the epidermis of SKH1 hairless mice. Together, our results show for the first time that p53-mediated GADD45α upregulation is the key mechanism by which silibinin protects against UVB-induced photodamage and provides a strong rationale to investigate silibinin in reducing the risk and/or preventing early onset of NMSC.
    MeSH term(s) Animals ; Apoptosis/genetics ; Apoptosis/radiation effects ; Cell Cycle/drug effects ; Cell Cycle Proteins/biosynthesis ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Line, Tumor ; Mice ; Mice, Hairless ; Nuclear Proteins/biosynthesis ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Pyrimidine Dimers/chemistry ; RNA Interference ; RNA, Small Interfering ; S Phase Cell Cycle Checkpoints ; Silybin ; Silymarin/pharmacology ; Skin/drug effects ; Skin/pathology ; Skin/radiation effects ; Skin Neoplasms/drug therapy ; Skin Neoplasms/prevention & control ; Tumor Suppressor Protein p53/biosynthesis ; Tumor Suppressor Protein p53/metabolism ; Ultraviolet Rays
    Chemical Substances Cell Cycle Proteins ; Gadd45a protein, mouse ; Nuclear Proteins ; Pyrimidine Dimers ; RNA, Small Interfering ; Silymarin ; Tumor Suppressor Protein p53 ; Silybin (4RKY41TBTF)
    Language English
    Publishing date 2011-12-12
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 603134-1
    ISSN 1460-2180 ; 0143-3334
    ISSN (online) 1460-2180
    ISSN 0143-3334
    DOI 10.1093/carcin/bgr299
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1558: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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