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  1. Article ; Online: Retraction Note: Inhibition of Tumor Angiogenesis by Tumstatin: Insights into Signaling Mechanisms and Implications in Cancer Regression.

    Sudhakar, Akulapalli / Boosani, Chandra S

    Pharmaceutical research

    2021  Volume 38, Issue 2, Page(s) 377

    Language English
    Publishing date 2021-02-08
    Publishing country United States
    Document type Retraction of Publication
    ZDB-ID 843063-9
    ISSN 1573-904X ; 0724-8741 ; 0739-0742
    ISSN (online) 1573-904X
    ISSN 0724-8741 ; 0739-0742
    DOI 10.1007/s11095-020-02974-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: History of Cancer, Ancient and Modern Treatment Methods.

    Sudhakar, Akulapalli

    Journal of cancer science & therapy

    2010  Volume 1, Issue 2, Page(s) 1–4

    Language English
    Publishing date 2010-07-30
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2578254-X
    ISSN 1948-5956
    ISSN 1948-5956
    DOI 10.4172/1948-5956.100000e2
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  3. Article ; Online: Human α1 type IV collagen NC1 domain exhibits distinct antiangiogenic activity mediated by α1β1 integrin.

    Sudhakar, Akulapalli / Nyberg, Pia / Keshamouni, Venkateshwar G / Mannam, Arjuna P / Li, Jian / Sugimoto, Hikaru / Cosgrove, Dominic / Kalluri, Raghu

    The Journal of clinical investigation

    2020  Volume 130, Issue 1, Page(s) 552

    Language English
    Publishing date 2020-02-06
    Publishing country United States
    Document type Journal Article ; Retraction of Publication
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI135305
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Molecular Cloning and Functional Characterization of Mouse α3(IV)NC1.

    Boosani, Chandra Shekhar / Sudhakar, Akulapalli

    Clinical medicine. Oncology

    2008  Volume 2, Page(s) 73–81

    Abstract: Non-collagenous α3 chain of type IV collagen or α3(IV)NC1, a 28 kDa C-terminal domain of collagen type IV is a specific inhibitor of endothelial cell translation and angiogenesis. In the present study we have cloned and expressed mouse α3(IV)NC1 in ... ...

    Abstract Non-collagenous α3 chain of type IV collagen or α3(IV)NC1, a 28 kDa C-terminal domain of collagen type IV is a specific inhibitor of endothelial cell translation and angiogenesis. In the present study we have cloned and expressed mouse α3(IV)NC1 in baculovirus system. The recombinant protein was expressed in soluble form and tested for several of its biological functions. We identified that this recombinant mouse α3(IV)NC1 specifically inhibited proliferation, translation and tube formation of endothelial cells. Also, we show that α3(IV)NC1 treatment results in apoptosis specifically in proliferating endothelial cells. In addition we report for the first time that mouse α3(IV)NC1 inhibits migration and p38 MAPK phosphorylation in addition to inhibition of FAK/Akt/mTOR/4E-BP1 signaling. In mice α3(IV)NC1 treatment reduced tumor growth and CD-31 positive endothelial vasculature in tumors. Collectively, our data demonstrate the expression of biologically active form of mouse α3(IV)NC1 in Sf-9 cells and provide important mechanistic insights on α3(IV)NC1 antiangiogenic actions in endothelial cells.
    Language English
    Publishing date 2008-02-09
    Publishing country New Zealand
    Document type Journal Article
    ZDB-ID 2517164-1
    ISSN 1177-9314
    ISSN 1177-9314
    DOI 10.4137/cmo.s461
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  5. Article ; Online: Molecular Cloning and Functional Characterization of Mouse α3(IV)NC1

    Chandra Shekhar Boosani / Akulapalli Sudhakar

    Clinical Medicine Insights : Oncology, Vol 2, Pp 73-

    2008  Volume 81

    Abstract: Non-collagenous α3 chain of type IV collagen or α3(IV)NC1, a 28 kDa C-terminal domain of collagen type IV is a specific inhibitor of endothelial cell translation and angiogenesis. In the present study we have cloned and expressed mouse α3(IV)NC1 in ... ...

    Abstract Non-collagenous α3 chain of type IV collagen or α3(IV)NC1, a 28 kDa C-terminal domain of collagen type IV is a specific inhibitor of endothelial cell translation and angiogenesis. In the present study we have cloned and expressed mouse α3(IV)NC1 in baculovirus system. The recombinant protein was expressed in soluble form and tested for several of its biological functions. We identified that this recombinant mouse α3(IV)NC1 specifically inhibited proliferation, translation and tube formation of endothelial cells. Also, we show that α3(IV)NC1 treatment results in apoptosis specifically in proliferating endothelial cells. In addition we report for the fi rst time that mouse α3(IV)NC1 inhibits migration and p38 MAPK phosphorylation in addition to inhibition of FAK/Akt/mTOR/4E-BP1 signaling. In mice α3(IV)NC1 treatment reduced tumor growth and CD-31 positive endothelial vasculature in tumors. Collectively, our data demonstrate the expression of biologically active form of mouse α3(IV)NC1 in Sf-9 cells and provide important mechanistic insights on α3(IV)NC1 antiangiogenic actions in endothelial cells.
    Keywords α3(IV)NC1 ; non-collagenous α3 chain of type IV collagen ; AcNPV ; Autographa californica nuclear polyhedrosis virus ; Sf-9 ; Spodoptera frugiperda ; MLEC ; mouse lung endothelial cells ; HUVEC ; human umbilical vein endothelial cells ; FCS ; fetal calf serum ; PMSF ; Phenylmethylsulfonyl Fluoride ; TNF-α ; tumor necrosis factor alpha ; DEVD ; cell membrane permeable caspase inhibitor ; NC ; negative control ; PC ; positive control ; FN ; fi bronectin ; MAPK ; mitogen activated protein kinase ; FAK ; focal adhesion kinase ; PKB/Akt ; protein kinase B ; mTOR ; mammalian target of rapamycin ; 4E-BP1 ; eukaryotic initiation factor 4E-binding protein ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Oncology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Language English
    Publishing date 2008-01-01T00:00:00Z
    Publisher Libertas Academica
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article: Inhibition of tumor angiogenesis by tumstatin: insights into signaling mechanisms and implications in cancer regression.

    Sudhakar, Akulapalli / Boosani, Chandra S

    publication RETRACTED

    Pharmaceutical research

    2008  Volume 25, Issue 12, Page(s) 2731–2739

    Abstract: Growing tumors develop additional new blood vessels to meet the demand for adequate nutrients and oxygen, a process called angiogenesis. Cancer is a highly complex disease promoted by excess angiogenesis; interfering with this process poses for an ... ...

    Abstract Growing tumors develop additional new blood vessels to meet the demand for adequate nutrients and oxygen, a process called angiogenesis. Cancer is a highly complex disease promoted by excess angiogenesis; interfering with this process poses for an attractive approach for controlling tumor growth. This hypothesis led to the identification of endogenous angiogenesis inhibitors generated from type IV collagen, a major component of vascular basement membrane (VBM). Type IV collagen and the angiogenesis inhibitors derived from it are involved in complex roles, than just the molecular construction of basement membranes. Protease degradation of collagens in VBM occurs in various physiological and pathological conditions and produces several peptides. Some of these peptides are occupied in the regulation of functions conflicting from those of their original integral molecules. Tumstatin (alpha3(IV)NC1), a proteolytic C-terminal non-collagenous (NC1) domain from type IV collagen alpha3 chain has been highlighted recently because of its potential role in anti-angiogenesis, however its biological actions are not limited to these processes. alpha3(IV)NC1 inhibits proliferation by promoting endothelial cell apoptosis and suppresses diverse tumor angiogenesis, thus making it a potential candidate for future cancer therapy. The present review surveys the physiological functions of type IV collagen and discovery of alpha3(IV)NC1 as an antiangiogenic protein with a comprehensive overview of the knowledge gained by us towards understanding its signaling mechanisms.
    MeSH term(s) Angiogenesis Inhibitors/pharmacology ; Animals ; Autoantigens/pharmacology ; Autoantigens/therapeutic use ; Collagen Type IV/pharmacology ; Collagen Type IV/physiology ; Collagen Type IV/therapeutic use ; Humans ; Integrin alpha3beta1/physiology ; Integrin alphaVbeta3/physiology ; Neoplasms/blood supply ; Neoplasms/drug therapy ; Neovascularization, Pathologic/prevention & control ; Signal Transduction/physiology
    Chemical Substances Angiogenesis Inhibitors ; Autoantigens ; Collagen Type IV ; Integrin alpha3beta1 ; Integrin alphaVbeta3 ; type IV collagen alpha3 chain
    Language English
    Publishing date 2008-06-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review ; Retracted Publication
    ZDB-ID 843063-9
    ISSN 1573-904X ; 0724-8741 ; 0739-0742
    ISSN (online) 1573-904X
    ISSN 0724-8741 ; 0739-0742
    DOI 10.1007/s11095-008-9634-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1937: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: Signaling mechanisms of endogenous angiogenesis inhibitors derived from type IV collagen.

    Sudhakar, Akulapalli / Boosani, Chandra S

    Gene regulation and systems biology

    2007  Volume 1, Page(s) 217–226

    Abstract: Vascular basement membrane (VBM) derived molecules are regulators of certain biological activities such as cell growth, differentiation and angiogenesis. Angiogenesis is regulated by a systematic controlled balance between VBM derived antiangiogenic ... ...

    Abstract Vascular basement membrane (VBM) derived molecules are regulators of certain biological activities such as cell growth, differentiation and angiogenesis. Angiogenesis is regulated by a systematic controlled balance between VBM derived antiangiogenic factors and proangiogenic growth factors. In the normal physiological state, equilibrium is maintained between the antiangiogenic and proangiogenic factors. The antiangiogenic factors (molecules), which are generated by the proteolytic cleavage of the VBM, include; alpha1 chain non-collagenous (NC1) domain of type XVIII collagen (endostatin) and the NC1 domains from the alpha chains of Type IV collagen considered as endogenous angiogenesis inhibitors. These collagen derived NC1 domains have a pivotal role in the regulation of tumor angiogenesis, thus making them attractive alternate candidates for cancer therapies. In this review we illustrate a comprehensive overview of the knowledge gained from the signaling mechanisms of Type IV collagen derived endogenous inhibitors in angiogenesis.
    Language English
    Publishing date 2007-10-14
    Publishing country United States
    Document type Journal Article
    ISSN 1177-6250
    ISSN (online) 1177-6250
    DOI 10.4137/grsb.s345
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Signaling Mechanisms of Endogenous Angiogenesis Inhibitors Derived from Type IV Collagen

    Akulapalli Sudhakar / Chandra S. Boosani

    Gene Regulation and Systems Biology, Vol 1, Pp 217-

    2007  Volume 226

    Abstract: Vascular basement membrane (VBM) derived molecules are regulators of certain biological activities such as cell growth, differentiation and angiogenesis. Angiogenesis is regulated by a systematic controlled balance between VBM derived antiangiogenic ... ...

    Abstract Vascular basement membrane (VBM) derived molecules are regulators of certain biological activities such as cell growth, differentiation and angiogenesis. Angiogenesis is regulated by a systematic controlled balance between VBM derived antiangiogenic factors and proangiogenic growth factors. In the normal physiological state, equilibrium is maintained between the antiangiogenic and proangiogenic factors. The antiangiogenic factors (molecules), which are generated by the proteolytic cleavage of the VBM, include; α1 chain non-collagenous (NC1) domain of type XVIII collagen (endostatin) and the NC1 domains from the alpha chains of Type IV collagen considered as endogenous angiogenesis inhibitors. These collagen derived NC1 domains have a pivotal role in the regulation of tumor angiogenesis, thus making them attractive alternate candidates for cancer therapies. In this review we illustrate a comprehensive overview of the knowledge gained from the signaling mechanisms of Type IV collagen derived endogenous inhibitors in angiogenesis.
    Keywords VBM ; vascular basement membrane ; ECM ; extra cellular matrix ; MMP ; matrix metalloproteinase ; HUVEC ; human umbilical vein endothelial cell ; MLEC ; mouse lung endothelial cells ; SCC-PSA1 ; teratocarcinoma cell line ; VEGF ; vascular endothelial cell growth factor ; bFGF ; basic fi broblast growth factor ; α1–α6(IV)NC1 ; non-collagenous α1–α6 chains of Type IV collagen domains ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2007-01-01T00:00:00Z
    Publisher SAGE Publishing
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article: Role of Chemokines and Chemokine Receptors in Prostate Cancer Development and Progression.

    Singh, Rajendra K / Sudhakar, Akulapalli / Lokeshwar, Bal L

    Journal of cancer science & therapy

    2010  Volume 2, Issue 4, Page(s) 89–94

    Abstract: Prostate cancer (PC) is the second leading cause of cancer deaths in men in America and Western Europe. Epidemiological studies suggest that prostate cancer incidences increased in last few years in Asian. The causes or consequences of increasing trend ... ...

    Abstract Prostate cancer (PC) is the second leading cause of cancer deaths in men in America and Western Europe. Epidemiological studies suggest that prostate cancer incidences increased in last few years in Asian. The causes or consequences of increasing trend of prostate cancer incidence are not completely known. Emerging evidences suggest that among the many risk factors, inflammation is the major risk factor for developing prostate cancer and its progression to metastasis. It is proposed that exposure to environmental factors such as infectious agents, dietary agents and saturated lipids leads to injury of the prostate due to chronic inflammation and regenerative risk factor lesions referred to as proliferative inflammatory atrophy (PIA). These phenomena predominantly control by a number of proinflammatory macro molecules such as chemokines, and their receptors. Some recent studies suggest that many of these pro-inflammatory chemokines and their receptors are the products of protooncogenes in many cancers including that of the prostate. This review will focus on the current biology of chemokines and chemokine receptors in prostate cancer. An understanding of this axis may enable researchers to develop targeted strategies for prostate cancer.
    Language English
    Publishing date 2010-08-27
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2578254-X
    ISSN 1948-5956
    ISSN 1948-5956
    DOI 10.4172/1948-5956.1000030
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  10. Article: Cloning, purification, and characterization of a non-collagenous anti-angiogenic protein domain from human alpha1 type IV collagen expressed in Sf9 cells.

    Boosani, Chandra Shekhar / Sudhakar, Akulapalli

    Protein expression and purification

    2006  Volume 49, Issue 2, Page(s) 211–218

    Abstract: alpha1(IV)NC1, a cleavage fragment of the carboxy terminal non-collagenous human alpha1 chain of type IV collagen, is derived from the extracellular matrix specifically by MMP-2. Recently we determined the in vitro and in vivo anti-angiogenic activity of ...

    Abstract alpha1(IV)NC1, a cleavage fragment of the carboxy terminal non-collagenous human alpha1 chain of type IV collagen, is derived from the extracellular matrix specifically by MMP-2. Recently we determined the in vitro and in vivo anti-angiogenic activity of alpha1(IV)NC1 and presently, its role in cancer therapy is under evaluation. To characterize alpha1(IV)NC1 as a potential candidate for drug development and to test its efficacy in animal models, an effective method to produce a purified active form of alpha1(IV)NC1 is needed. In the present study, expression of alpha1(IV)NC1 in Sf9 cells using baculovirus expression system was discussed, this method was found to be effective in the production of a functionally active soluble form of the recombinant protein. The purified protein showed its characteristic activities such as inhibiting cell proliferation, migration, and tube formation in endothelial cells.
    MeSH term(s) Angiogenesis Inhibitors/genetics ; Angiogenesis Inhibitors/isolation & purification ; Angiogenesis Inhibitors/pharmacology ; Angiogenesis Inhibitors/therapeutic use ; Animals ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Cloning, Molecular ; Collagen Type IV/genetics ; Collagen Type IV/isolation & purification ; Collagen Type IV/pharmacology ; Collagen Type IV/therapeutic use ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Gene Expression ; Humans ; Neoplasms/drug therapy ; Neovascularization, Pathologic/drug therapy ; Protein Structure, Tertiary/genetics ; Recombinant Proteins/genetics ; Recombinant Proteins/isolation & purification ; Recombinant Proteins/pharmacology ; Recombinant Proteins/therapeutic use ; Spodoptera/cytology
    Chemical Substances Angiogenesis Inhibitors ; Collagen Type IV ; Recombinant Proteins
    Language English
    Publishing date 2006-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1055455-5
    ISSN 1096-0279 ; 1046-5928
    ISSN (online) 1096-0279
    ISSN 1046-5928
    DOI 10.1016/j.pep.2006.03.007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 3084: Show issues Location:
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