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  1. AU=Kreger Bridget T.
  2. AU="Woods, Angela L"
  3. AU=Iba Toshiaki
  4. AU="Akberova, N I"
  5. AU="Bolouki Moghaddam, Farzaneh"
  6. AU="Rajeshkannan, Nadarajah"
  7. AU="Noda, Judith"
  8. AU=Loucks Catrina M.
  9. AU="Lachérade, J-C"
  10. AU=Jalali Subhadra AU=Jalali Subhadra
  11. AU="Yang, Yung"
  12. AU="Belt, Brian"
  13. AU="Beckley, Akinpelumi A"
  14. AU="Adams, Tempe"
  15. AU=Wahidi Momen M
  16. AU="Pardis C. Sabeti"
  17. AU=Arkowitz Robert A
  18. AU="Sempoux, Christine"
  19. AU="Selebatso, Moses"
  20. AU=Sountoulides Petros
  21. AU="Huachun Zou"
  22. AU=SHENG Nan AU=SHENG Nan
  23. AU="Gascon, Pierre"
  24. AU="Hoa Phong, Pham Huu Thien"
  25. AU="Guiyan Ni"

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  1. Artikel: The Enrichment of Survivin in Exosomes from Breast Cancer Cells Treated with Paclitaxel Promotes Cell Survival and Chemoresistance.

    Kreger, Bridget T / Johansen, Eric R / Cerione, Richard A / Antonyak, Marc A

    Cancers

    2016  Band 8, Heft 12

    Abstract: The generation and release of membrane-enclosed packets from cancer cells, called extracellular vesicles (EVs), play important roles in propagating transformed phenotypes, including promoting cell survival. EVs mediate their effects by transferring their ...

    Abstract The generation and release of membrane-enclosed packets from cancer cells, called extracellular vesicles (EVs), play important roles in propagating transformed phenotypes, including promoting cell survival. EVs mediate their effects by transferring their contents, which include specific proteins and nucleic acids, to target cells. However, how the cargo and function of EVs change in response to different stimuli remains unclear. Here, we discovered that treating highly aggressive MDAMB231 breast cancer cells with paclitaxel (PTX), a chemotherapy that stabilizes microtubules, causes them to generate a specific class of EV, namely exosomes, that are highly enriched with the cell survival protein and cancer marker, Survivin. Treating MDAMB231 cells with a variety of other chemotherapeutic agents, and inhibitors that block cell growth and survival, did not have the same effect as PTX, with the exception of nocodazole, another inhibitor of microtubule dynamics. Exosomes isolated from PTX-treated MDAMB231 cells strongly promoted the survival of serum-starved and PTX-treated fibroblasts and SKBR3 breast cancer cells, an effect that was ablated when Survivin was knocked-down from these vesicles using siRNA. These findings underscore how the enrichment of a specific cargo in exosomes promotes cell survival, as well as can potentially serve as a marker of PTX resistance.
    Sprache Englisch
    Erscheinungsdatum 2016-12-09
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers8120111
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Microvesicle Cargo and Function Changes upon Induction of Cellular Transformation.

    Kreger, Bridget T / Dougherty, Andrew L / Greene, Kai Su / Cerione, Richard A / Antonyak, Marc A

    The Journal of biological chemistry

    2016  Band 291, Heft 38, Seite(n) 19774–19785

    Abstract: Extracellular vesicles (EVs), including exosomes and microvesicles (MVs), have emerged as a major form of intercellular communication, playing important roles in several physiological processes and diseases, including cancer. EVs generated by cancer ... ...

    Abstract Extracellular vesicles (EVs), including exosomes and microvesicles (MVs), have emerged as a major form of intercellular communication, playing important roles in several physiological processes and diseases, including cancer. EVs generated by cancer cells contain a variety of proteins and RNA species that can be transferred between cancer cells as well as between cancer and non-transformed (normal) cells, thereby impacting a number of aspects of cancer progression. Here we show how oncogenic transformation influences the biogenesis and function of EVs using a mouse embryonic fibroblast (MEF) cell line that can be induced to express an oncogenic form of diffuse B cell lymphoma (Dbl). Although MEFs induced to express onco-Dbl generated a similar amount of MVs as uninduced control cells, we found that MVs isolated from onco-Dbl-transformed cells contain a unique signaling protein, the ubiquitously expressed non-receptor tyrosine kinase focal adhesion kinase. The addition of MVs isolated from MEFs expressing onco-Dbl to cultures of fibroblasts strongly promoted their survival and induced their ability to grow under anchorage-independent conditions, outcomes that could be reversed by knocking down focal adhesion kinase and depleting it from the MVs or by inhibiting its kinase activity using a specific inhibitor. We then showed the same to be true for MVs isolated from aggressive MDAMB231 breast cancer cells. Together, these findings demonstrate that the induction of oncogenic transformation gives rise to MVs, which uniquely contain a signaling protein kinase that helps propagate the transformed phenotype and thus may offer a specific diagnostic marker of malignant disease.
    Mesh-Begriff(e) Animals ; Cell Line, Tumor ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Cell-Derived Microparticles/genetics ; Cell-Derived Microparticles/metabolism ; Embryo, Mammalian/metabolism ; Exosomes/genetics ; Exosomes/metabolism ; Female ; Gene Expression Regulation, Neoplastic/genetics ; Guanine Nucleotide Exchange Factors/genetics ; Guanine Nucleotide Exchange Factors/metabolism ; Humans ; Mice ; NIH 3T3 Cells ; Neoplasms/genetics ; Neoplasms/metabolism ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism
    Chemische Substanzen Guanine Nucleotide Exchange Factors ; MCF2 protein, human ; Mcf2 protein, mouse ; Proto-Oncogene Proteins
    Sprache Englisch
    Erscheinungsdatum 2016-07-20
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M116.725705
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: The Enrichment of Survivin in Exosomes from Breast Cancer Cells Treated with Paclitaxel Promotes Cell Survival and Chemoresistance

    Bridget T. Kreger / Eric R. Johansen / Richard A. Cerione / Marc A. Antonyak

    Cancers, Vol 8, Iss 12, p

    2016  Band 111

    Abstract: The generation and release of membrane-enclosed packets from cancer cells, called extracellular vesicles (EVs), play important roles in propagating transformed phenotypes, including promoting cell survival. EVs mediate their effects by transferring their ...

    Abstract The generation and release of membrane-enclosed packets from cancer cells, called extracellular vesicles (EVs), play important roles in propagating transformed phenotypes, including promoting cell survival. EVs mediate their effects by transferring their contents, which include specific proteins and nucleic acids, to target cells. However, how the cargo and function of EVs change in response to different stimuli remains unclear. Here, we discovered that treating highly aggressive MDAMB231 breast cancer cells with paclitaxel (PTX), a chemotherapy that stabilizes microtubules, causes them to generate a specific class of EV, namely exosomes, that are highly enriched with the cell survival protein and cancer marker, Survivin. Treating MDAMB231 cells with a variety of other chemotherapeutic agents, and inhibitors that block cell growth and survival, did not have the same effect as PTX, with the exception of nocodazole, another inhibitor of microtubule dynamics. Exosomes isolated from PTX-treated MDAMB231 cells strongly promoted the survival of serum-starved and PTX-treated fibroblasts and SKBR3 breast cancer cells, an effect that was ablated when Survivin was knocked-down from these vesicles using siRNA. These findings underscore how the enrichment of a specific cargo in exosomes promotes cell survival, as well as can potentially serve as a marker of PTX resistance.
    Schlagwörter intercellular communication ; exosomes ; cell signaling ; tumor microenvironment ; extracellular vesicles ; Survivin ; chemotherapy ; chemoresistance ; paclitaxel ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R
    Sprache Englisch
    Erscheinungsdatum 2016-12-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

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  4. Artikel ; Online: α-catenin is a tumor suppressor that controls cell accumulation by regulating the localization and activity of the transcriptional coactivator Yap1.

    Silvis, Mark R / Kreger, Bridget T / Lien, Wen-Hui / Klezovitch, Olga / Rudakova, G Marianna / Camargo, Fernando D / Lantz, Dan M / Seykora, John T / Vasioukhin, Valeri

    Science signaling

    2011  Band 4, Heft 174, Seite(n) ra33

    Abstract: The Hippo pathway regulates contact inhibition of cell proliferation and, ultimately, organ size in diverse multicellular organisms. Inactivation of the Hippo pathway promotes nuclear localization of the transcriptional coactivator Yap1, a Hippo pathway ... ...

    Abstract The Hippo pathway regulates contact inhibition of cell proliferation and, ultimately, organ size in diverse multicellular organisms. Inactivation of the Hippo pathway promotes nuclear localization of the transcriptional coactivator Yap1, a Hippo pathway effector, and can cause cancer. Here, we show that deletion of αE (α epithelial) catenin in the hair follicle stem cell compartment resulted in the development of skin squamous cell carcinoma in mice. Tumor formation was accelerated by simultaneous deletion of αE-catenin and the tumor suppressor-encoding gene p53. A small interfering RNA screen revealed a functional connection between αE-catenin and Yap1. By interacting with Yap1, αE-catenin promoted its cytoplasmic localization, and Yap1 showed constitutive nuclear localization in αE-catenin-null cells. We also found an inverse correlation between αE-catenin abundance and Yap1 activation in human squamous cell carcinoma tumors. These findings identify αE-catenin as a tumor suppressor that inhibits Yap1 activity and sequesters it in the cytoplasm.
    Mesh-Begriff(e) Active Transport, Cell Nucleus/genetics ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/metabolism ; Carcinoma, Squamous Cell/pathology ; Cell Cycle Proteins ; Cell Line, Tumor ; Cell Nucleus/genetics ; Cell Nucleus/metabolism ; Cell Proliferation ; HEK293 Cells ; Humans ; Mice ; Mice, Nude ; Mice, Transgenic ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Transcription Factors ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; alpha Catenin/genetics ; alpha Catenin/metabolism
    Chemische Substanzen Adaptor Proteins, Signal Transducing ; Cell Cycle Proteins ; Phosphoproteins ; TP53 protein, human ; Transcription Factors ; Tumor Suppressor Protein p53 ; YAP1 protein, human ; Yap1 protein, mouse ; alpha Catenin
    Sprache Englisch
    Erscheinungsdatum 2011-05-24
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2417226-1
    ISSN 1937-9145 ; 1945-0877
    ISSN (online) 1937-9145
    ISSN 1945-0877
    DOI 10.1126/scisignal.2001823
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Yap1 acts downstream of α-catenin to control epidermal proliferation.

    Schlegelmilch, Karin / Mohseni, Morvarid / Kirak, Oktay / Pruszak, Jan / Rodriguez, J Renato / Zhou, Dawang / Kreger, Bridget T / Vasioukhin, Valera / Avruch, Joseph / Brummelkamp, Thijn R / Camargo, Fernando D

    Cell

    2011  Band 144, Heft 5, Seite(n) 782–795

    Abstract: During development and regeneration, proliferation of tissue-specific stem cells is tightly controlled to produce organs of a predetermined size. The molecular determinants of this process remain poorly understood. Here, we investigate the function of ... ...

    Abstract During development and regeneration, proliferation of tissue-specific stem cells is tightly controlled to produce organs of a predetermined size. The molecular determinants of this process remain poorly understood. Here, we investigate the function of Yap1, the transcriptional effector of the Hippo signaling pathway, in skin biology. Using gain- and loss-of-function studies, we show that Yap1 is a critical modulator of epidermal stem cell proliferation and tissue expansion. Yap1 mediates this effect through interaction with TEAD transcription factors. Additionally, our studies reveal that α-catenin, a molecule previously implicated in tumor suppression and cell density sensing in the skin, is an upstream negative regulator of Yap1. α-catenin controls Yap1 activity and phosphorylation by modulating its interaction with 14-3-3 and the PP2A phosphatase. Together, these data identify Yap1 as a determinant of the proliferative capacity of epidermal stem cells and as an important effector of a "crowd control" molecular circuitry in mammalian skin.
    Mesh-Begriff(e) 14-3-3 Proteins/metabolism ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Cell Cycle Proteins ; Cell Line ; Cell Proliferation ; Epidermal Cells ; Epidermis/metabolism ; Mice ; Phosphoproteins/metabolism ; alpha Catenin/metabolism
    Chemische Substanzen 14-3-3 Proteins ; Adaptor Proteins, Signal Transducing ; Cell Cycle Proteins ; Phosphoproteins ; Yap1 protein, mouse ; alpha Catenin
    Sprache Englisch
    Erscheinungsdatum 2011-03-02
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2011.02.031
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel: Yap1 Acts Downstream of α-Catenin to Control Epidermal Proliferation

    Schlegelmilch, Karin / Mohseni, Morvarid / Kirak, Oktay / Pruszak, Jan / Rodriguez, J. Renato / Zhou, Dawang / Kreger, Bridget T / Vasioukhin, Valera / Avruch, Joseph / Brummelkamp, Thijn R / Camargo, Fernando D

    Cell. 2011 Mar. 4, v. 144, no. 5

    2011  

    Abstract: During development and regeneration, proliferation of tissue-specific stem cells is tightly controlled to produce organs of a predetermined size. The molecular determinants of this process remain poorly understood. Here, we investigate the function of ... ...

    Abstract During development and regeneration, proliferation of tissue-specific stem cells is tightly controlled to produce organs of a predetermined size. The molecular determinants of this process remain poorly understood. Here, we investigate the function of Yap1, the transcriptional effector of the Hippo signaling pathway, in skin biology. Using gain- and loss-of-function studies, we show that Yap1 is a critical modulator of epidermal stem cell proliferation and tissue expansion. Yap1 mediates this effect through interaction with TEAD transcription factors. Additionally, our studies reveal that α-catenin, a molecule previously implicated in tumor suppression and cell density sensing in the skin, is an upstream negative regulator of Yap1. α-catenin controls Yap1 activity and phosphorylation by modulating its interaction with 14-3-3 and the PP2A phosphatase. Together, these data identify Yap1 as a determinant of the proliferative capacity of epidermal stem cells and as an important effector of a “crowd control” molecular circuitry in mammalian skin.
    Schlagwörter cell proliferation ; epidermis (animal) ; mammals ; phosphoprotein phosphatase ; protein phosphorylation ; protein-protein interactions ; signal transduction ; stem cells ; transcription (genetics) ; transcription factors
    Sprache Englisch
    Erscheinungsverlauf 2011-0304
    Umfang p. 782-795.
    Erscheinungsort Elsevier Inc.
    Dokumenttyp Artikel
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2011.02.031
    Datenquelle NAL Katalog (AGRICOLA)

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  7. Artikel ; Online: Long-range energy transport in single supramolecular nanofibres at room temperature.

    Haedler, Andreas T / Kreger, Klaus / Issac, Abey / Wittmann, Bernd / Kivala, Milan / Hammer, Natalie / Köhler, Jürgen / Schmidt, Hans-Werner / Hildner, Richard

    Nature

    2015  Band 523, Heft 7559, Seite(n) 196–199

    Abstract: ... by one-dimensional self-assembly of supramolecular building blocks, based on carbonyl-bridged ...

    Abstract Efficient transport of excitation energy over long distances is a key process in light-harvesting systems, as well as in molecular electronics. However, in synthetic disordered organic materials, the exciton diffusion length is typically only around 10 nanometres (refs 4, 5), or about 50 nanometres in exceptional cases, a distance that is largely determined by the probability laws of incoherent exciton hopping. Only for highly ordered organic systems has the transport of excitation energy over macroscopic distances been reported--for example, for triplet excitons in anthracene single crystals at room temperature, as well as along single polydiacetylene chains embedded in their monomer crystalline matrix at cryogenic temperatures (at 10 kelvin, or -263 degrees Celsius). For supramolecular nanostructures, uniaxial long-range transport has not been demonstrated at room temperature. Here we show that individual self-assembled nanofibres with molecular-scale diameter efficiently transport singlet excitons at ambient conditions over more than four micrometres, a distance that is limited only by the fibre length. Our data suggest that this remarkable long-range transport is predominantly coherent. Such coherent long-range transport is achieved by one-dimensional self-assembly of supramolecular building blocks, based on carbonyl-bridged triarylamines, into well defined H-type aggregates (in which individual monomers are aligned cofacially) with substantial electronic interactions. These findings may facilitate the development of organic nanophotonic devices and quantum information technology.
    Sprache Englisch
    Erscheinungsdatum 2015-07-09
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/nature14570
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel: Yap1 Acts Downstream of α-Catenin to Control Epidermal Proliferation

    Schlegelmilch, Karin / Mohseni, Morvarid / Kirak, Oktay / Pruszak, Jan / Rodriguez, J. Renato / Zhou, Dawang / Kreger, Bridget T. / Vasioukhin, Valera / Avruch, Joseph / Brummelkamp, Thijn R. / Camargo, Fernando D.

    Cell

    Band v. 144,, Heft no. 5

    Abstract: During development and regeneration, proliferation of tissue-specific stem cells is tightly controlled to produce organs of a predetermined size. The molecular determinants of this process remain poorly understood. Here, we investigate the function of ... ...

    Abstract During development and regeneration, proliferation of tissue-specific stem cells is tightly controlled to produce organs of a predetermined size. The molecular determinants of this process remain poorly understood. Here, we investigate the function of Yap1, the transcriptional effector of the Hippo signaling pathway, in skin biology. Using gain- and loss-of-function studies, we show that Yap1 is a critical modulator of epidermal stem cell proliferation and tissue expansion. Yap1 mediates this effect through interaction with TEAD transcription factors. Additionally, our studies reveal that α-catenin, a molecule previously implicated in tumor suppression and cell density sensing in the skin, is an upstream negative regulator of Yap1. α-catenin controls Yap1 activity and phosphorylation by modulating its interaction with 14-3-3 and the PP2A phosphatase. Together, these data identify Yap1 as a determinant of the proliferative capacity of epidermal stem cells and as an important effector of a “crowd control” molecular circuitry in mammalian skin.
    Schlagwörter mammals ; protein-protein interactions ; protein phosphorylation ; cell proliferation ; phosphoprotein phosphatase ; stem cells ; epidermis (animal) ; transcription factors ; signal transduction ; transcription (genetics)
    Sprache Englisch
    Dokumenttyp Artikel
    ISSN 0092-8674
    Datenquelle AGRIS - International Information System for the Agricultural Sciences and Technology

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