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  1. Article ; Online: The 4th International p63/p73 workshop: p53's (older) sisters take centre stage.

    Basu, S / Kadakia, M P

    Cell death and differentiation

    2009  Volume 17, Issue 3, Page(s) 562–564

    MeSH term(s) Animals ; Congresses as Topic ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Humans ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Neoplasms/genetics ; Neoplasms/metabolism ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Tumor Protein p73 ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism
    Chemical Substances CKAP4 protein, human ; DNA-Binding Proteins ; Membrane Proteins ; Nuclear Proteins ; TP73 protein, human ; Trp73 protein, mouse ; Tumor Protein p73 ; Tumor Suppressor Protein p53 ; Tumor Suppressor Proteins
    Language English
    Publishing date 2009-11-06
    Publishing country England
    Document type Journal Article
    ZDB-ID 1225672-9
    ISSN 1476-5403 ; 1350-9047
    ISSN (online) 1476-5403
    ISSN 1350-9047
    DOI 10.1038/cdd.2009.170
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Human herpesvirus 6 infection and associated pathogenesis following bone marrow transplantation.

    Kadakia, M P

    Leukemia & lymphoma

    1998  Volume 31, Issue 3-4, Page(s) 251–266

    Abstract: Human herpesvirus 6 (HHV-6) infections following bone marrow transplantation (BMT) have been shown to be associated with fever, skin rash, graft versus host disease, encephalitis, delay in engraftment, marrow suppression, and pneumonia. Unfortunately ... ...

    Abstract Human herpesvirus 6 (HHV-6) infections following bone marrow transplantation (BMT) have been shown to be associated with fever, skin rash, graft versus host disease, encephalitis, delay in engraftment, marrow suppression, and pneumonia. Unfortunately several of these studies were case reports and although the results were suggestive they prompted us to study these pathological events systematically. These associations were primarily based on either HHV-6 isolation, HHV-6 DNA detection, antigen detection or increases in HHV-6 specific antibodies. HHV-6 activity was more frequent during the post- rather than the pre-transplantation period. All HHV-6 isolates from BMT patients have been shown to be variant B. A better understanding of HHV-6 associated pathogenesis gained by larger prospective trials is needed to facilitate proper treatment of cases of idiopathic illnesses or those associated with symptoms (fever, skin rash) similar to those caused by HHV-6.
    MeSH term(s) Bone Marrow Transplantation/adverse effects ; Herpesviridae Infections/etiology ; Herpesviridae Infections/physiopathology ; Herpesvirus 6, Human/isolation & purification ; Humans
    Language English
    Publishing date 1998-10
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1042374-6
    ISSN 1029-2403 ; 1042-8194
    ISSN (online) 1029-2403
    ISSN 1042-8194
    DOI 10.3109/10428199809059218
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The 5th International p63/p73 Workshop: much more than just tumour suppression.

    Kadakia, M P / Caron de Fromentel, C / de-Fromentel, C C / Sabapathy, K

    Cell death and differentiation

    2012  Volume 19, Issue 3, Page(s) 549–550

    MeSH term(s) Animals ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Disease Models, Animal ; Education ; France ; Genome-Wide Association Study ; Humans ; Mice ; Mice, Mutant Strains ; Mutation ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Tumor Protein p73 ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism
    Chemical Substances DNA-Binding Proteins ; Nuclear Proteins ; Phosphoproteins ; TP63 protein, human ; TP73 protein, human ; Trans-Activators ; Transcription Factors ; Trp63 protein, mouse ; Trp73 protein, mouse ; Tumor Protein p73 ; Tumor Suppressor Proteins
    Language English
    Publishing date 2012-01-13
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1225672-9
    ISSN 1476-5403 ; 1350-9047
    ISSN (online) 1476-5403
    ISSN 1350-9047
    DOI 10.1038/cdd.2011.204
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: p73 is essential for vitamin D-mediated osteoblastic differentiation.

    Kommagani, R / Whitlatch, A / Leonard, M K / Kadakia, M P

    Cell death and differentiation

    2009  Volume 17, Issue 3, Page(s) 398–407

    Abstract: The secosteroid hormone vitamin D3 (VD3) exerts its biological actions through its cognate receptor, the vitamin D receptor (VDR). Vitamin D3 and VDR have a key function in bone formation and keratinocyte differentiation, exert antiproliferative actions ... ...

    Abstract The secosteroid hormone vitamin D3 (VD3) exerts its biological actions through its cognate receptor, the vitamin D receptor (VDR). Vitamin D3 and VDR have a key function in bone formation and keratinocyte differentiation, exert antiproliferative actions in human cancer, and is widely used as a chemotherapeutic agent for cancer. In addition, VD3 promotes differentiation of human osteosarcoma cells by up-regulating genes involved in cell cycle arrest and osteoblastic differentiation. Although considerable work has been carried out in understanding the molecular mechanisms underlying the VD3-mediated differentiation of human osteosarcoma cells, the upstream regulation of VD3 signaling pathway is still unclear. In this study, we show that p73 acts as an upstream regulator of VD3-mediated osteoblastic differentiation. Transcription factor p73, a p53 homolog, has been shown to have a function in development and recently been termed as a tumor suppressor. Silencing p73 results in a significant reduction of VD3-mediated osteoblastic differentiation; although DNA damage induced p73 leads to an increase in VD3-mediated differentiation of osteosarcoma cells. Together, our data implicate a novel function for p73 in vitamin D-mediated differentiation of human osteosarcoma cells.
    MeSH term(s) Cell Differentiation/drug effects ; Cell Differentiation/physiology ; Cell Line, Tumor ; DNA Damage ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Humans ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Osteoblasts/cytology ; Osteoblasts/drug effects ; Osteoblasts/physiology ; Osteocalcin/genetics ; Osteocalcin/metabolism ; Osteopontin/genetics ; Osteopontin/metabolism ; Osteosarcoma/genetics ; Osteosarcoma/metabolism ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Receptors, Calcitriol/genetics ; Receptors, Calcitriol/metabolism ; Signal Transduction/physiology ; Tumor Protein p73 ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism ; Vitamin D/pharmacology
    Chemical Substances DNA-Binding Proteins ; Nuclear Proteins ; RNA, Small Interfering ; Receptors, Calcitriol ; TP73 protein, human ; Tumor Protein p73 ; Tumor Suppressor Proteins ; Osteocalcin (104982-03-8) ; Osteopontin (106441-73-0) ; Vitamin D (1406-16-2)
    Language English
    Publishing date 2009-09-25
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1225672-9
    ISSN 1476-5403 ; 1350-9047
    ISSN (online) 1476-5403
    ISSN 1350-9047
    DOI 10.1038/cdd.2009.135
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Identification of vitamin D receptor as a target of p63.

    Kommagani, R / Caserta, T M / Kadakia, M P

    Oncogene

    2006  Volume 25, Issue 26, Page(s) 3745–3751

    Abstract: p63, a p53 homolog has been shown to play a role in development and cancer. p63 is essential for both commitment of ectoderm to stratified epithelia and for the proliferative potential of epithelial stem cells. p63 knockout mice are born with severe ... ...

    Abstract p63, a p53 homolog has been shown to play a role in development and cancer. p63 is essential for both commitment of ectoderm to stratified epithelia and for the proliferative potential of epithelial stem cells. p63 knockout mice are born with severe development defects and lack organs of epithelial origin. In addition, p63 has also been shown to play a role in cancer development through the differential regulation of genes with tumor suppressor function and genes involved in metastasis. In order to understand the role of p63 in cancer and development, genes that are specifically regulated by p63 but not p53 were identified. In this study, we provide evidence that p63gamma specifically upregulates vitamin D Receptor (VDR). In contrast, p53 does not appear to be involved in upregulation of VDR expression. Additionally, we demonstrate that a naturally occurring p63 missense mutant, p63gamma (R279H) and p14(ARF), both act in a dominant negative manner to inhibit p63gamma-mediated upregulation of VDR. Furthermore, using chromatin immunoprecipitation assays, we demonstrated that p63 directly binds to the VDR promoter in vivo. Our findings clearly demonstrate that VDR is a direct target of p63 and suggests that p63 may play a role in cancer and differentiation through modulation of the VDR pathway.
    MeSH term(s) Bone Neoplasms/genetics ; Bone Neoplasms/pathology ; Cell Differentiation/genetics ; Chromatin Immunoprecipitation ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation ; HeLa Cells ; Humans ; Mutation, Missense ; Osteosarcoma/genetics ; Osteosarcoma/pathology ; Promoter Regions, Genetic ; Receptors, Calcitriol/genetics ; Receptors, Calcitriol/metabolism ; Response Elements ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Transcription Factors ; Tumor Cells, Cultured ; Tumor Suppressor Protein p14ARF/genetics ; Tumor Suppressor Protein p14ARF/metabolism ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism
    Chemical Substances DNA-Binding Proteins ; Receptors, Calcitriol ; TP63 protein, human ; Trans-Activators ; Transcription Factors ; Tumor Suppressor Protein p14ARF ; Tumor Suppressor Proteins
    Language English
    Publishing date 2006-06-22
    Publishing country England
    Document type Journal Article
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/sj.onc.1209412
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2218: Show issues Location:
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  6. Article ; Online: ΔNp63α regulates keratinocyte proliferation by controlling PTEN expression and localization.

    Leonard, M K / Kommagani, R / Payal, V / Mayo, L D / Shamma, H N / Kadakia, M P

    Cell death and differentiation

    2011  Volume 18, Issue 12, Page(s) 1924–1933

    Abstract: ΔNp63α, implicated as an oncogene, is upregulated by activated Akt, part of a well-known cell survival pathway. Inhibition of Akt activation by phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and the presence of putative p63-binding sites ... ...

    Abstract ΔNp63α, implicated as an oncogene, is upregulated by activated Akt, part of a well-known cell survival pathway. Inhibition of Akt activation by phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and the presence of putative p63-binding sites in the pten promoter led us to investigate whether ΔNp63α regulates PTEN expression. Knockdown of ΔNp63α led to increases in PTEN levels and loss of activated Akt, while overexpression of ΔNp63α decreased PTEN levels and elevated active Akt. The repression of PTEN by ΔNp63α occurs independently of p53 status, as loss of ΔNp63α increases PTEN expression in cell lines with and without functional p53. In addition, decreased levels of ΔNp63α resulted in an increase in nuclear PTEN. Conversely, in vivo nuclear PTEN was absent in the proliferative basal layer of the epidermis where ΔNp63α expression is highest. Additionally, we show that in keratinocytes a balance between ΔNp63α and PTEN regulates Akt activation and maintains normal proliferation rates. This balance is disrupted in non-melanoma skin cancers through increased ΔNp63α levels, and could enhance proliferation and subsequent neoplastic development. Our studies show that ΔNp63α negatively regulates PTEN, thereby providing a feedback loop between PTEN, Akt and ΔNp63α, which has an integral role in skin cancer development.
    MeSH term(s) Animals ; Base Sequence ; Carcinoma, Basal Cell/metabolism ; Carcinoma, Basal Cell/pathology ; Carcinoma, Squamous Cell/metabolism ; Carcinoma, Squamous Cell/pathology ; Cell Nucleus/metabolism ; Cell Proliferation ; Cells, Cultured ; Down-Regulation ; Enzyme Activation ; Feedback, Physiological ; Gene Expression ; Gene Expression Regulation ; Humans ; Keratinocytes/metabolism ; Keratinocytes/physiology ; Mice ; Molecular Sequence Data ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/metabolism ; Protein Transport ; Proto-Oncogene Proteins c-akt/metabolism ; Response Elements ; Skin/metabolism ; Skin Neoplasms/metabolism ; Skin Neoplasms/pathology ; Transcription Factors/metabolism ; Tumor Suppressor Proteins/metabolism
    Chemical Substances TP63 protein, human ; Transcription Factors ; Tumor Suppressor Proteins ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; PTEN protein, human (EC 3.1.3.67)
    Language English
    Publishing date 2011-06-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1225672-9
    ISSN 1476-5403 ; 1350-9047
    ISSN (online) 1476-5403
    ISSN 1350-9047
    DOI 10.1038/cdd.2011.73
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Human herpesvirus 6: infection and disease following autologous and allogeneic bone marrow transplantation.

    Kadakia, M P / Rybka, W B / Stewart, J A / Patton, J L / Stamey, F R / Elsawy, M / Pellett, P E / Armstrong, J A

    Blood

    1996  Volume 87, Issue 12, Page(s) 5341–5354

    Abstract: Human herpesvirus 6 activity (HHV-6) was studied in 15 allogeneic and 11 autologous marrow transplantation patients. After transplantation, HHV-6 was isolated from the peripheral blood mononuclear cells of 12 of 26 patients (6 allogeneic and 6 autologous) ...

    Abstract Human herpesvirus 6 activity (HHV-6) was studied in 15 allogeneic and 11 autologous marrow transplantation patients. After transplantation, HHV-6 was isolated from the peripheral blood mononuclear cells of 12 of 26 patients (6 allogeneic and 6 autologous). All isolates were variant B. Eleven of 26 and 12 of 19 patients showed salivary shedding of HHV-6 DNA before and after transplantation, respectively. The antibody titer increased in 7 of 26 patients. Thus, 23 of 26 patients showed evidence of active HHV-6 infection either by virus isolation, salivary shedding, or increases in antibody titers. The fraction of saliva specimens positive in 19 patients was negatively associated with their antibody titers (P= .005). The proportion of cultures positive increased after transplantation (P = .007). Sinusitis was associated with HHV-6 isolation in autologous recipients (P= .002). In allogeneic patients, active human cytomegalovirus infection was associated with HHV-6 isolation (P = .04). No association was observed between HHV-6 infection and GVHD, pneumonia, delay in engraftment, or marrow suppression. Of the 120 clinical events analyzed in 26 patients, HHV-6 was defined as a probable cause of 16 events in 9 patients based on the propinquity of HHV-6 activity and the clinical event plus the absence of other identified causes of the event.
    MeSH term(s) Adult ; Base Sequence ; Bone Marrow Transplantation/adverse effects ; Breast Neoplasms/epidemiology ; Breast Neoplasms/therapy ; Comorbidity ; Cytomegalovirus Infections/epidemiology ; DNA, Viral/analysis ; Female ; Graft vs Host Disease/epidemiology ; Herpes Zoster/epidemiology ; Herpesviridae Infections/epidemiology ; Herpesviridae Infections/etiology ; Herpesvirus 6, Human/classification ; Herpesvirus 6, Human/isolation & purification ; Herpesvirus 6, Human/physiology ; Humans ; Immunosuppression/adverse effects ; Infections/epidemiology ; Leukemia/epidemiology ; Leukemia/therapy ; Leukocytes, Mononuclear/virology ; Life Tables ; Lymphoma/epidemiology ; Lymphoma/therapy ; Male ; Middle Aged ; Molecular Sequence Data ; Ovarian Neoplasms/epidemiology ; Ovarian Neoplasms/therapy ; Pennsylvania/epidemiology ; Pilot Projects ; Prospective Studies ; Sinusitis/epidemiology ; Sinusitis/virology ; Survival Analysis ; Transplantation, Autologous/adverse effects ; Transplantation, Homologous/adverse effects ; Treatment Outcome ; Virus Activation
    Chemical Substances DNA, Viral
    Language English
    Publishing date 1996-06-15
    Publishing country United States
    Document type Comparative Study ; Journal Article
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    Database MEDical Literature Analysis and Retrieval System OnLINE

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