ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    Promoting axon regeneration in the adult CNS by modulation of the PTEN/mTOR pathway (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-08
    Description: The failure of axons to regenerate is a major obstacle for functional recovery after central nervous system (CNS) injury. Removing extracellular inhibitory molecules results in limited axon regeneration in vivo. To test for the role of intrinsic impediments to axon regrowth, we analyzed cell growth control genes using a virus-assisted in vivo conditional knockout approach. Deletion of PTEN (phosphatase and tensin homolog), a negative regulator of the mammalian target of rapamycin (mTOR) pathway, in adult retinal ganglion cells (RGCs) promotes robust axon regeneration after optic nerve injury. In wild-type adult mice, the mTOR activity was suppressed and new protein synthesis was impaired in axotomized RGCs, which may contribute to the regeneration failure. Reactivating this pathway by conditional knockout of tuberous sclerosis complex 1, another negative regulator of the mTOR pathway, also leads to axon regeneration. Thus, our results suggest the manipulation of intrinsic growth control pathways as a therapeutic approach to promote axon regeneration after CNS injury.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652400/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652400/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Kevin Kyungsuk -- Liu, Kai -- Hu, Yang -- Smith, Patrice D -- Wang, Chen -- Cai, Bin -- Xu, Bengang -- Connolly, Lauren -- Kramvis, Ioannis -- Sahin, Mustafa -- He, Zhigang -- R01 NS051788/NS/NINDS NIH HHS/ -- R01 NS051788-04/NS/NINDS NIH HHS/ -- R01 NS058956/NS/NINDS NIH HHS/ -- R01 NS058956-02/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 Nov 7;322(5903):963-6. doi: 10.1126/science.1161566.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉F. M. Kirby Neurobiology Center, Children's Hospital, and Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18988856" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Axotomy ; Carrier Proteins/*metabolism ; Cell Survival ; Mice ; Mice, Knockout ; Nerve Crush ; *Nerve Regeneration ; Optic Nerve ; PTEN Phosphohydrolase/genetics/*metabolism ; Phosphotransferases (Alcohol Group Acceptor)/*metabolism ; Protein Biosynthesis ; Retinal Ganglion Cells/metabolism/physiology ; Ribosomal Protein S6/metabolism ; *Signal Transduction ; TOR Serine-Threonine Kinases ; Tumor Suppressor Proteins/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    EGFR activation mediates inhibition of axon regeneration by myelin and chondroitin sulfate proteoglycans (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-08
    Description: Inhibitory molecules associated with myelin and the glial scar limit axon regeneration in the adult central nervous system (CNS), but the underlying signaling mechanisms of regeneration inhibition are not fully understood. Here, we show that suppressing the kinase function of the epidermal growth factor receptor (EGFR) blocks the activities of both myelin inhibitors and chondroitin sulfate proteoglycans in inhibiting neurite outgrowth. In addition, regeneration inhibitors trigger the phosphorylation of EGFR in a calcium-dependent manner. Local administration of EGFR inhibitors promotes significant regeneration of injured optic nerve fibers, pointing to a promising therapeutic avenue for enhancing axon regeneration after CNS injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koprivica, Vuk -- Cho, Kin-Sang -- Park, Jong Bae -- Yiu, Glenn -- Atwal, Jasvinder -- Gore, Bryan -- Kim, Jieun A -- Lin, Estelle -- Tessier-Lavigne, Marc -- Chen, Dong Feng -- He, Zhigang -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):106-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/drug effects/*physiology ; Calcium/metabolism ; Cells, Cultured ; Chondroitin Sulfate Proteoglycans/*metabolism ; Enzyme Inhibitors/pharmacology ; Erlotinib Hydrochloride ; GPI-Linked Proteins ; Humans ; Mice ; Myelin Proteins/*metabolism/pharmacology ; Nerve Crush ; *Nerve Regeneration/drug effects ; Neurites/drug effects/physiology ; Optic Nerve/drug effects/physiology ; Optic Nerve Injuries/drug therapy ; Phosphorylation ; Quinazolines/pharmacology ; Receptor, Epidermal Growth Factor/*antagonists & inhibitors/*metabolism ; Receptors, Cell Surface/metabolism ; Retinal Ganglion Cells/drug effects/physiology ; Signal Transduction/drug effects ; Tyrphostins/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Induction of functional hepatocyte-like cells from mouse fibroblasts by defined factors (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-05-13
    Description: The generation of functional hepatocytes independent of donor liver organs is of great therapeutic interest with regard to regenerative medicine and possible cures for liver disease. Induced hepatic differentiation has been achieved previously using embryonic stem cells or induced pluripotent stem cells. Particularly, hepatocytes generated from a patient's own induced pluripotent stem cells could theoretically avoid immunological rejection. However, the induction of hepatocytes from induced pluripotent stem cells is a complicated process that would probably be replaced with the arrival of improved technology. Overexpression of lineage-specific transcription factors directly converts terminally differentiated cells into some other lineages, including neurons, cardiomyocytes and blood progenitors; however, it remains unclear whether these lineage-converted cells could repair damaged tissues in vivo. Here we demonstrate the direct induction of functional hepatocyte-like (iHep) cells from mouse tail-tip fibroblasts by transduction of Gata4, Hnf1alpha and Foxa3, and inactivation of p19(Arf). iHep cells show typical epithelial morphology, express hepatic genes and acquire hepatocyte functions. Notably, transplanted iHep cells repopulate the livers of fumarylacetoacetate-hydrolase-deficient (Fah(-/-)) mice and rescue almost half of recipients from death by restoring liver functions. Our study provides a novel strategy to generate functional hepatocyte-like cells for the purpose of liver engineering and regenerative medicine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Pengyu -- He, Zhiying -- Ji, Shuyi -- Sun, Huawang -- Xiang, Dao -- Liu, Changcheng -- Hu, Yiping -- Wang, Xin -- Hui, Lijian -- England -- Nature. 2011 May 11;475(7356):386-9. doi: 10.1038/nature10116.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy for Sciences, Yueyang Road 320, 200031 Shanghai, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21562492" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation/genetics ; Cell Lineage ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p16/deficiency/genetics ; DNA-Binding Proteins/deficiency ; Fibroblasts/*cytology/*metabolism ; GATA4 Transcription Factor/genetics/metabolism ; Gene Expression Profiling ; Hepatocyte Nuclear Factor 1-alpha/genetics/metabolism ; Hepatocyte Nuclear Factor 3-gamma/genetics/metabolism ; Hepatocytes/*cytology/*metabolism/physiology/transplantation ; Hydrolases/deficiency/genetics ; Liver/cytology/enzymology/physiology/physiopathology ; Liver Diseases/enzymology/pathology/physiopathology/therapy ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Regenerative Medicine/methods ; Survival Rate ; Tail/cytology ; Tissue Engineering/methods ; Transduction, Genetic
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    Cortical representations of olfactory input by trans-synaptic tracing (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-12-24
    Description: In the mouse, each class of olfactory receptor neurons expressing a given odorant receptor has convergent axonal projections to two specific glomeruli in the olfactory bulb, thereby creating an odour map. However, it is unclear how this map is represented in the olfactory cortex. Here we combine rabies-virus-dependent retrograde mono-trans-synaptic labelling with genetics to control the location, number and type of 'starter' cortical neurons, from which we trace their presynaptic neurons. We find that individual cortical neurons receive input from multiple mitral cells representing broadly distributed glomeruli. Different cortical areas represent the olfactory bulb input differently. For example, the cortical amygdala preferentially receives dorsal olfactory bulb input, whereas the piriform cortex samples the whole olfactory bulb without obvious bias. These differences probably reflect different functions of these cortical areas in mediating innate odour preference or associative memory. The trans-synaptic labelling method described here should be widely applicable to mapping connections throughout the mouse nervous system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3073090/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3073090/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyamichi, Kazunari -- Amat, Fernando -- Moussavi, Farshid -- Wang, Chen -- Wickersham, Ian -- Wall, Nicholas R -- Taniguchi, Hiroki -- Tasic, Bosiljka -- Huang, Z Josh -- He, Zhigang -- Callaway, Edward M -- Horowitz, Mark A -- Luo, Liqun -- R01 MH063912/MH/NIMH NIH HHS/ -- R01 NS050835/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Apr 14;472(7342):191-6. doi: 10.1038/nature09714. Epub 2010 Dec 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉HHMI/Department of Biology, Stanford University, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179085" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/anatomy & histology/cytology/physiology ; Animals ; Axons/physiology ; Bias (Epidemiology) ; Brain Mapping ; HEK293 Cells ; Humans ; Mice ; Mice, Transgenic ; *Neuroanatomical Tract-Tracing Techniques ; Odors/analysis ; Olfactory Bulb/anatomy & histology/cytology/physiology ; Olfactory Pathways/anatomy & histology/*cytology/*physiology ; Olfactory Perception/genetics/*physiology ; Olfactory Receptor Neurons/cytology/physiology ; Rabies virus/physiology ; Synapses/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    Sustained axon regeneration induced by co-deletion of PTEN and SOCS3 (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-11-08
    Description: A formidable challenge in neural repair in the adult central nervous system (CNS) is the long distances that regenerating axons often need to travel in order to reconnect with their targets. Thus, a sustained capacity for axon regeneration is critical for achieving functional restoration. Although deletion of either phosphatase and tensin homologue (PTEN), a negative regulator of mammalian target of rapamycin (mTOR), or suppressor of cytokine signalling 3 (SOCS3), a negative regulator of Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway, in adult retinal ganglion cells (RGCs) individually promoted significant optic nerve regeneration, such regrowth tapered off around 2 weeks after the crush injury. Here we show that, remarkably, simultaneous deletion of both PTEN and SOCS3 enables robust and sustained axon regeneration. We further show that PTEN and SOCS3 regulate two independent pathways that act synergistically to promote enhanced axon regeneration. Gene expression analyses suggest that double deletion not only results in the induction of many growth-related genes, but also allows RGCs to maintain the expression of a repertoire of genes at the physiological level after injury. Our results reveal concurrent activation of mTOR and STAT3 pathways as key for sustaining long-distance axon regeneration in adult CNS, a crucial step towards functional recovery.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240702/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240702/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Fang -- Park, Kevin K -- Belin, Stephane -- Wang, Dongqing -- Lu, Tao -- Chen, Gang -- Zhang, Kang -- Yeung, Cecil -- Feng, Guoping -- Yankner, Bruce A -- He, Zhigang -- DP1 AG044161/AG/NIA NIH HHS/ -- R01 EY018660/EY/NEI NIH HHS/ -- R01 EY021342/EY/NEI NIH HHS/ -- R01 EY021342-01A1/EY/NEI NIH HHS/ -- R01 EY021374/EY/NEI NIH HHS/ -- R01 EY021526/EY/NEI NIH HHS/ -- R01 EY021526-01/EY/NEI NIH HHS/ -- England -- Nature. 2011 Nov 6;480(7377):372-5. doi: 10.1038/nature10594.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉F.M. Kirby Neurobiology Center, Children's Hospital, Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22056987" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/pathology/*physiology ; Cell Growth Processes/genetics ; Gene Expression Regulation ; Mice ; Mice, Inbred C57BL ; Nerve Crush ; Nerve Regeneration/*physiology ; Optic Nerve/cytology/growth & development/pathology ; Optic Nerve Injuries/genetics/metabolism/pathology ; PTEN Phosphohydrolase/*deficiency/genetics ; Retinal Ganglion Cells/metabolism ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; Suppressor of Cytokine Signaling Proteins/*deficiency/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    PTPsigma is a receptor for chondroitin sulfate proteoglycan, an inhibitor of neural regeneration (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-17
    Description: Chondroitin sulfate proteoglycans (CSPGs) present a barrier to axon regeneration. However, no specific receptor for the inhibitory effect of CSPGs has been identified. We showed that a transmembrane protein tyrosine phosphatase, PTPsigma, binds with high affinity to neural CSPGs. Binding involves the chondroitin sulfate chains and a specific site on the first immunoglobulin-like domain of PTPsigma. In culture, PTPsigma(-/-) neurons show reduced inhibition by CSPG. A PTPsigma fusion protein probe can detect cognate ligands that are up-regulated specifically at neural lesion sites. After spinal cord injury, PTPsigma gene disruption enhanced the ability of axons to penetrate regions containing CSPG. These results indicate that PTPsigma can act as a receptor for CSPGs and may provide new therapeutic approaches to neural regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811318/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811318/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, Yingjie -- Tenney, Alan P -- Busch, Sarah A -- Horn, Kevin P -- Cuascut, Fernando X -- Liu, Kai -- He, Zhigang -- Silver, Jerry -- Flanagan, John G -- R01 EY011559/EY/NEI NIH HHS/ -- R01 NS025713/NS/NINDS NIH HHS/ -- R37 HD029417/HD/NICHD NIH HHS/ -- R37 NS025713/NS/NINDS NIH HHS/ -- R37 NS025713-22/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 23;326(5952):592-6. doi: 10.1126/science.1178310. Epub 2009 Oct 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19833921" target="_blank"〉PubMed〈/a〉
    Keywords: Aggrecans/metabolism ; Animals ; Astrocytes/metabolism ; Axons/physiology ; Binding Sites ; Cells, Cultured ; Chondroitin Sulfate Proteoglycans/chemistry/*metabolism ; Chondroitin Sulfates/metabolism ; Female ; Ganglia, Spinal/cytology/metabolism ; Ligands ; Mice ; *Nerve Regeneration ; Nerve Tissue Proteins/chemistry/*metabolism ; Neurites/physiology ; Neurons/*physiology ; Protein Binding ; Protein Interaction Domains and Motifs ; Proteoglycans/chemistry/*metabolism ; Receptor-Like Protein Tyrosine Phosphatases, Class ; 2/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Spinal Cord/metabolism/pathology ; Spinal Cord Injuries/*metabolism/pathology/physiopathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...