Connection

JUAN BOTAS to Nerve Tissue Proteins

This is a "connection" page, showing publications JUAN BOTAS has written about Nerve Tissue Proteins.
Connection Strength

1.198
  1. Suppression of neurodegeneration and increased neurotransmission caused by expanded full-length huntingtin accumulating in the cytoplasm. Neuron. 2008 Jan 10; 57(1):27-40.
    View in: PubMed
    Score: 0.184
  2. Identification of genes that modify ataxin-1-induced neurodegeneration. Nature. 2000 Nov 02; 408(6808):101-6.
    View in: PubMed
    Score: 0.112
  3. Integrated genomics and proteomics define huntingtin CAG length-dependent networks in mice. Nat Neurosci. 2016 Apr; 19(4):623-33.
    View in: PubMed
    Score: 0.081
  4. Huntingtin proteolysis releases non-polyQ fragments that cause toxicity through dynamin 1 dysregulation. EMBO J. 2015 Sep 02; 34(17):2255-71.
    View in: PubMed
    Score: 0.077
  5. Targeting ATM ameliorates mutant Huntingtin toxicity in cell and animal models of Huntington's disease. Sci Transl Med. 2014 Dec 24; 6(268):268ra178.
    View in: PubMed
    Score: 0.074
  6. RAS-MAPK-MSK1 pathway modulates ataxin 1 protein levels and toxicity in SCA1. Nature. 2013 Jun 20; 498(7454):325-331.
    View in: PubMed
    Score: 0.067
  7. Identification of NUB1 as a suppressor of mutant Huntington toxicity via enhanced protein clearance. Nat Neurosci. 2013 May; 16(5):562-70.
    View in: PubMed
    Score: 0.066
  8. A genome-scale RNA-interference screen identifies RRAS signaling as a pathologic feature of Huntington's disease. PLoS Genet. 2012; 8(11):e1003042.
    View in: PubMed
    Score: 0.064
  9. Network organization of the huntingtin proteomic interactome in mammalian brain. Neuron. 2012 Jul 12; 75(1):41-57.
    View in: PubMed
    Score: 0.063
  10. Inhibition of lipid signaling enzyme diacylglycerol kinase epsilon attenuates mutant huntingtin toxicity. J Biol Chem. 2012 Jun 15; 287(25):21204-13.
    View in: PubMed
    Score: 0.062
  11. Matrix metalloproteinases are modifiers of huntingtin proteolysis and toxicity in Huntington's disease. Neuron. 2010 Jul 29; 67(2):199-212.
    View in: PubMed
    Score: 0.055
  12. dAtaxin-2 mediates expanded Ataxin-1-induced neurodegeneration in a Drosophila model of SCA1. PLoS Genet. 2007 Dec 28; 3(12):e234.
    View in: PubMed
    Score: 0.045
  13. Huntingtin interacting proteins are genetic modifiers of neurodegeneration. PLoS Genet. 2007 May 11; 3(5):e82.
    View in: PubMed
    Score: 0.044
  14. ATAXIN-1 interacts with the repressor Capicua in its native complex to cause SCA1 neuropathology. Cell. 2006 Dec 29; 127(7):1335-47.
    View in: PubMed
    Score: 0.043
  15. CHIP protects from the neurotoxicity of expanded and wild-type ataxin-1 and promotes their ubiquitination and degradation. J Biol Chem. 2006 Sep 08; 281(36):26714-24.
    View in: PubMed
    Score: 0.041
  16. The AXH domain of Ataxin-1 mediates neurodegeneration through its interaction with Gfi-1/Senseless proteins. Cell. 2005 Aug 26; 122(4):633-44.
    View in: PubMed
    Score: 0.039
  17. Interaction of Akt-phosphorylated ataxin-1 with 14-3-3 mediates neurodegeneration in spinocerebellar ataxia type 1. Cell. 2003 May 16; 113(4):457-68.
    View in: PubMed
    Score: 0.033
  18. The LIM homeodomain protein dLim1 defines a subclass of neurons within the embryonic ventral nerve cord of Drosophila. Mech Dev. 1999 Nov; 88(2):195-205.
    View in: PubMed
    Score: 0.026
  19. Comparative analysis of genetic modifiers in Drosophila points to common and distinct mechanisms of pathogenesis among polyglutamine diseases. Hum Mol Genet. 2008 Feb 01; 17(3):376-90.
    View in: PubMed
    Score: 0.011
  20. Neurotoxic protein expression reveals connections between the circadian clock and mating behavior in Drosophila. Proc Natl Acad Sci U S A. 2006 Sep 05; 103(36):13537-42.
    View in: PubMed
    Score: 0.010
Connection Strength

The connection strength for concepts is the sum of the scores for each matching publication.

Publication scores are based on many factors, including how long ago they were written and whether the person is a first or senior author.