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  1. Article: Basic fibroblast growth factor induces TGF-beta release in an isoform and glioma-specific manner.

    Dhandapani, Krishnan M / Wade, Marlene F / Mahesh, Virendra B / Brann, Darrell W

    Neuroreport

    2002  Volume 13, Issue 2, Page(s) 239–241

    Abstract: The aim of the current study was to determine whether basic fibroblast growth factor (bFGF), regulates the release of transforming growth factor-beta1 (TGF-beta1) from C6 glioma cells. The results of the study show that bFGF (2, 5 and 10 ng/ml) dose ... ...

    Abstract The aim of the current study was to determine whether basic fibroblast growth factor (bFGF), regulates the release of transforming growth factor-beta1 (TGF-beta1) from C6 glioma cells. The results of the study show that bFGF (2, 5 and 10 ng/ml) dose dependently induced the release of TGF-beta1 from C6 glioma cells, with the 10 ng/ml dose inducing a 2- to 3-fold increase of TGF-beta1 levels. This effect was evident as early as 6 h following treatment, with maximal levels observed at 18 h. The effect of bFGF was largely on latent TGF-beta1, and was isoform specific, as bFGF had no effect on TGF-beta2 release. The bFGF effect on TGF-beta1 was also glioma specific, as no such stimulatory effect was observed in rat cortical astrocytes.
    MeSH term(s) Animals ; Astrocytes/drug effects ; Astrocytes/metabolism ; Cerebral Cortex/cytology ; Cerebral Cortex/drug effects ; Cerebral Cortex/metabolism ; Dose-Response Relationship, Drug ; Fibroblast Growth Factor 2/administration & dosage ; Fibroblast Growth Factor 2/pharmacology ; Glioma/metabolism ; Protein Isoforms/metabolism ; Rats ; Time Factors ; Transforming Growth Factor beta/metabolism ; Tumor Cells, Cultured
    Chemical Substances Protein Isoforms ; Transforming Growth Factor beta ; Fibroblast Growth Factor 2 (103107-01-3)
    Language English
    Publishing date 2002-02-11
    Publishing country England
    Document type Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 1049746-8
    ISSN 1473-558X ; 0959-4965
    ISSN (online) 1473-558X
    ISSN 0959-4965
    DOI 10.1097/00001756-200202110-00013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3118: Show issues Location:
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  2. Article ; Online: Receptor-mediated delivery of engineered nucleases for genome modification.

    Chen, Zhong / Jaafar, Lahcen / Agyekum, Davies G / Xiao, Haiyan / Wade, Marlene F / Kumaran, R Ileng / Spector, David L / Bao, Gang / Porteus, Matthew H / Dynan, William S / Meiler, Steffen E

    Nucleic acids research

    2013  Volume 41, Issue 19, Page(s) e182

    Abstract: Engineered nucleases, which incise the genome at predetermined sites, have a number of laboratory and clinical applications. There is, however, a need for better methods for controlled intracellular delivery of nucleases. Here, we demonstrate a method ... ...

    Abstract Engineered nucleases, which incise the genome at predetermined sites, have a number of laboratory and clinical applications. There is, however, a need for better methods for controlled intracellular delivery of nucleases. Here, we demonstrate a method for ligand-mediated delivery of zinc finger nucleases (ZFN) proteins using transferrin receptor-mediated endocytosis. Uptake is rapid and efficient in established mammalian cell lines and in primary cells, including mouse and human hematopoietic stem-progenitor cell populations. In contrast to cDNA expression, ZFN protein levels decline rapidly following internalization, affording better temporal control of nuclease activity. We show that transferrin-mediated ZFN uptake leads to site-specific in situ cleavage of the target locus. Additionally, despite the much shorter duration of ZFN activity, the efficiency of gene correction approaches that seen with cDNA-mediated expression. The approach is flexible and general, with the potential for extension to other targeting ligands and nuclease architectures.
    MeSH term(s) Animals ; Cell Line ; Cells, Cultured ; DNA Cleavage ; Deoxyribonucleases/genetics ; Deoxyribonucleases/metabolism ; Endocytosis ; Genomics ; Humans ; Ligands ; Mice ; Protein Engineering ; Receptors, Transferrin/metabolism ; Recombinant Fusion Proteins/metabolism ; Targeted Gene Repair/methods ; Transferrin/genetics ; Transferrin/metabolism ; Zinc Fingers
    Chemical Substances Ligands ; Receptors, Transferrin ; Recombinant Fusion Proteins ; Transferrin ; Deoxyribonucleases (EC 3.1.-)
    Language English
    Publishing date 2013-08-16
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 186809-3
    ISSN 1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
    ISSN (online) 1362-4962 ; 1362-4954
    ISSN 0301-5610 ; 0305-1048
    DOI 10.1093/nar/gkt710
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1067: Show issues Location:
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  3. Article: Leptin and reproduction.

    Brann, Darrell W / Wade, Marlene F / Dhandapani, Krishnan M / Mahesh, Virendra B / Buchanan, Clint D

    Steroids

    2001  Volume 67, Issue 2, Page(s) 95–104

    Abstract: Since the cloning of leptin by Friedman's laboratory in 1994, over 3000 papers have been published on leptin, making it one of the most active research areas in all of science. Leptin appears to be a pleiotrophic hormone affecting many different tissues ... ...

    Abstract Since the cloning of leptin by Friedman's laboratory in 1994, over 3000 papers have been published on leptin, making it one of the most active research areas in all of science. Leptin appears to be a pleiotrophic hormone affecting many different tissues in the body. This review focuses on the role of leptin in reproduction. Evidence is accumulating that leptin potentially has roles in the regulation of GnRH and LH secretion, puberty, pregnancy, and lactation. Reciprocal regulation of leptin and its receptors by gonadal hormones and the implications and controversies thereof are also discussed in the review. Signaling pathways utilized by leptin are starting to become more clear, particularly JAK/STAT, MAPK, and SOCS3 have been implicated as mediators/modulators of leptin effects at the cellular level. At the hypothalamic level, there is also evidence that CART (cocaine and amphetamine-related transcript) is involved as a downstream mediator of leptin effects, especially with regards to control of GnRH secretion. While leptin clearly has many effects upon the reproductive axis, defining its precise roles is not without controversies. This review presents both pro and con findings, thereby demarking controversial areas that undoubtedly will be fertile ground for future investigation.
    MeSH term(s) Animals ; Carrier Proteins/metabolism ; Female ; Humans ; Lactation/metabolism ; Leptin/metabolism ; Neurosecretory Systems/metabolism ; Pregnancy ; Receptors, Cell Surface ; Receptors, Leptin ; Reproduction ; Signal Transduction ; Steroids/metabolism
    Chemical Substances Carrier Proteins ; LEPR protein, human ; Leptin ; Receptors, Cell Surface ; Receptors, Leptin ; Steroids
    Language English
    Publishing date 2001-01-01
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
    ZDB-ID 80312-1
    ISSN 1878-5867 ; 0039-128X
    ISSN (online) 1878-5867
    ISSN 0039-128X
    DOI 10.1016/s0039-128x(01)00138-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 87: Show issues Location:
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  4. Article: Astrocyte protection of neurons: role of transforming growth factor-beta signaling via a c-Jun-AP-1 protective pathway.

    Dhandapani, Krishnan M / Hadman, Martin / De Sevilla, Liesl / Wade, Marlene F / Mahesh, Virendra B / Brann, Darrell W

    The Journal of biological chemistry

    2003  Volume 278, Issue 44, Page(s) 43329–43339

    Abstract: Astrocytes have become a focal point for research in neurobiology, especially regarding their purported ability to regulate neuronal communication and survival. The present study addressed a poorly understood but important focus in this area, the ... ...

    Abstract Astrocytes have become a focal point for research in neurobiology, especially regarding their purported ability to regulate neuronal communication and survival. The present study addressed a poorly understood but important focus in this area, the mechanism(s) underlying astrocyte-induced survival of neurons. The results of the study show that soluble factors in astrocyte-conditioned media (ACM) protect murine GT1-7 neurons from serum deprivation-induced cell death and that this neuroprotection is correlated with enhanced activation/phosphorylation of the AP-1 transcription factor, c-JunSer-63. A parallel and correlated activation of the upstream kinases, c-Jun N-terminal kinase (JNK) and mitogen-activated protein kinase kinase-4 (MKK4) was also demonstrated. Furthermore, co-administration of JNK inhibitors, but not a MEK inhibitor, significantly attenuated ACM-induced phosphorylation of c-JunSer-63 and blocked its neuroprotective action. Gel shift analysis demonstrated that ACM enhanced AP-1 binding, an effect that appears functionally important, since an AP-1 binding inhibitor significantly attenuated the neuroprotective action of ACM. Further studies implicated transforming growth factor (TGF)-beta1 and TGF-beta2 as critical active soluble factors released by astrocytes, since both were demonstrated in ACM, and immunoneutralization of the conditioned media with a panspecific TGF-beta antibody significantly attenuated the enhanced AP-1 binding and neuroprotective action of the ACM. Furthermore, exogenous application of TGF-beta1 and TGF-beta2 was found to enhance c-JunSer-63 phosphorylation and to be neuroprotective, and co-administration of JNK inhibitors or an AP-1 binding inhibitor blocked TGF-beta-induced neuroprotection. Taken together, these studies suggest that astrocytes can protect neurons from serum deprivation-induced cell death, at least in part, by release of TGF-beta and activation of a c-Jun/AP-1 protective pathway.
    MeSH term(s) Animals ; Astrocytes/metabolism ; Blotting, Western ; Cell Line ; Cell Nucleus/metabolism ; Cell Survival ; Cells, Cultured ; Culture Media, Conditioned/pharmacology ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Genes, Dominant ; Mice ; Models, Biological ; Neurons/metabolism ; Phosphorylation ; Protein Binding ; Proto-Oncogene Proteins c-jun/metabolism ; Signal Transduction ; Swine ; Time Factors ; Transcription Factor AP-1/metabolism ; Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta/physiology
    Chemical Substances Culture Media, Conditioned ; Enzyme Inhibitors ; Proto-Oncogene Proteins c-jun ; Transcription Factor AP-1 ; Transforming Growth Factor beta
    Language English
    Publishing date 2003-07-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M305835200
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uc I Zs.108: Show issues Location:
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  5. Article ; Online: Direct Anterior Pituitary Modulation of Gonadotropin Secretion by Neuropeptide Y: Role of Gonadal Steroids

    O’Conner, James L. / Wade, Marlene F. / Brann, Darrell W. / Mahesh, Virendra B.

    Neuroendocrinology - International Journal for Basic and Clinical Studies on Neuroendocrine Relationships

    1993  Volume 58, Issue 1, Page(s) 129–135

    Abstract: Neuropeptide Y (NPY) acts at the hypothalamus to stimulate LH secretion through increased LHRH secretion. NPY is also cosecreted into the portal system in a pulsatile manner with LHRH and may act at the anterior pituitary to increase LH secretion through ...

    Abstract Neuropeptide Y (NPY) acts at the hypothalamus to stimulate LH secretion through increased LHRH secretion. NPY is also cosecreted into the portal system in a pulsatile manner with LHRH and may act at the anterior pituitary to increase LH secretion through potentiation of LHRH responsiveness and possibly through direct stimulation; however, controversy exists concerning this direct action of NPY at the pituitary. Utilizing dispersed anterior pituitary monolayer cell cultures, the first goal of this study was to determine the effects of vehicle, 10-10M LHRH, 10-7M NPY, 10-6M NPY, 10-10 M LHRH + 10-7M NPY, and 10-10M LHRH + 10-6M NPY on LH and FSH responsiveness. Under these conditions, 10-6M NPY alone significantly stimulated LH secretion (630% above basal) and both 10-7M NPY and 10-6 M NPY significantly potentiated LHRH-induced LH secretion (195 and 244% above LHRH alone, respectively). Neither 10-7M NPY nor 10-6M NPY alone stimulated FSH secretion; however, both 10-7M and 10-6M NPY significantly potentiated LHRH-induced FSH secretion (130 and 135% above LHRH alone, respectively). The second goal of this study was to determine whether the gonadal steroid conditions prevailing prior to the preovulatory gonadotropin surge play a role in modulating NPY responsiveness; this experiment utilized anterior pituitary (AP) halves from immature ovariectomized estrogen + progesterone (E + P) primed female rats to determine the role of gonadal steroids in the LH and FSH response to vehicle, 10-8M LHRH, 10-7M NPY, 10-6M NPY, 10-8M LHRH + 10-7M NPY, 10-8M LHRH + 10-6M NPY. Under these conditions, data indicated that NPY alone did not significantly stimulate LH secretion in this animal model. However, LHRH-induced LH release was potentiated by 10-6M NPY in vehicle, estrogen (E), and estrogen + progesterone primed groups (240, 160 and 200% above LHRH alone, respectively), while 10-7M NPY potentiated LHRH-induced LH release only in the estrogen and estrogen + progesterone-primed groups (150 and 170% greater than LHRH alone, respectively). Estrogen + progesterone did not significantly increase the magnitude of NPY potentiation above that observed in the estrogen only group. NPY alone did not stimulate FSH secretion in any group. Neither estrogen alone nor estrogen + progesterone had any effect on FSH responsiveness to NPY or LHRH alone; neither estrogen alone nor estrogen + progesterone potentiated LHRH-induced FSH secretion. These studies demonstrated that in dispersed AP cell cultures derived from intact random cycle rats, NPY was capable of acting either alone to stimulate LH secretion or in combination with LHRH to potentiate both LH and FSH secretion. When the immature ovariectomized E + P-primed rat model was employed, these studies demonstrated that estrogen alone in the absence of progesteron (P) was sufficient to maximize LH responsiveness to NPY + LHRH, thereby indicating that P probably acts at the hypothalamus in vivo to induce the gonadotropin surge observed in this model. The data support the hypothesis that NPY is a physiologically significant modulator of gonadotropin secretion.
    Keywords NPY ; LHRH ; Pituitary ; LH ; FSH
    Language English
    Publisher S. Karger AG
    Publishing place Basel
    Publishing country Switzerland
    Document type Article ; Online
    ZDB-ID 123303-8
    ISSN 1423-0194 ; 0028-3835 ; 0028-3835
    ISSN (online) 1423-0194
    ISSN 0028-3835
    DOI 10.1159/000126521
    Database Karger publisher's database

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