Connection

JUAN BOTAS to Disease Models, Animal

This is a "connection" page, showing publications JUAN BOTAS has written about Disease Models, Animal.
Connection Strength

0.882
  1. Drosophila researchers focus on human disease. Nat Genet. 2007 May; 39(5):589-91.
    View in: PubMed
    Score: 0.125
  2. Computational and functional prioritization identifies genes that rescue behavior and reduce tau protein in fly and human cell models of Alzheimer disease. Am J Hum Genet. 2025 May 01; 112(5):1081-1096.
    View in: PubMed
    Score: 0.108
  3. Mouse and fly models of neurodegeneration. Trends Genet. 2002 Sep; 18(9):463-71.
    View in: PubMed
    Score: 0.090
  4. Downregulation of glial genes involved in synaptic function mitigates Huntington's disease pathogenesis. Elife. 2021 04 19; 10.
    View in: PubMed
    Score: 0.082
  5. Network organization of the huntingtin proteomic interactome in mammalian brain. Neuron. 2012 Jul 12; 75(1):41-57.
    View in: PubMed
    Score: 0.045
  6. 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: 0.033
  7. RNA-binding proteins hnRNP A2/B1 and CUGBP1 suppress fragile X CGG premutation repeat-induced neurodegeneration in a Drosophila model of FXTAS. Neuron. 2007 Aug 16; 55(4):565-71.
    View in: PubMed
    Score: 0.032
  8. Multi-epitope immunocapture of huntingtin reveals striatum-selective molecular signatures. Mol Syst Biol. 2025 May; 21(5):492-522.
    View in: PubMed
    Score: 0.027
  9. Suppression of toxicity of the mutant huntingtin protein by its interacting compound, desonide. Proc Natl Acad Sci U S A. 2022 03 08; 119(10):e2114303119.
    View in: PubMed
    Score: 0.022
  10. Dynamics of huntingtin protein interactions in the striatum identifies candidate modifiers of Huntington disease. Cell Syst. 2022 04 20; 13(4):304-320.e5.
    View in: PubMed
    Score: 0.022
  11. Spinocerebellar Ataxia Type 1 protein Ataxin-1 is signaled to DNA damage by ataxia-telangiectasia mutated kinase. Hum Mol Genet. 2021 05 17; 30(8):706-715.
    View in: PubMed
    Score: 0.021
  12. Identification of genes that modify ataxin-1-induced neurodegeneration. Nature. 2000 Nov 02; 408(6808):101-6.
    View in: PubMed
    Score: 0.020
  13. Cross-species genetic screens to identify kinase targets for APP reduction in Alzheimer's disease. Hum Mol Genet. 2019 06 15; 28(12):2014-2029.
    View in: PubMed
    Score: 0.018
  14. PAK1 regulates ATXN1 levels providing an opportunity to modify its toxicity in spinocerebellar ataxia type 1. Hum Mol Genet. 2018 08 15; 27(16):2863-2873.
    View in: PubMed
    Score: 0.017
  15. High-Throughput Functional Analysis Distinguishes Pathogenic, Nonpathogenic, and Compensatory Transcriptional Changes in Neurodegeneration. Cell Syst. 2018 07 25; 7(1):28-40.e4.
    View in: PubMed
    Score: 0.017
  16. Inhibition of PIP4K? ameliorates the pathological effects of mutant huntingtin protein. Elife. 2017 12 26; 6.
    View in: PubMed
    Score: 0.016
  17. TRIM28 regulates the nuclear accumulation and toxicity of both alpha-synuclein and tau. Elife. 2016 10 25; 5.
    View in: PubMed
    Score: 0.015
  18. Reduction of Nuak1 Decreases Tau and Reverses Phenotypes in a Tauopathy Mouse Model. Neuron. 2016 Oct 19; 92(2):407-418.
    View in: PubMed
    Score: 0.015
  19. Metal Homeostasis Regulators Suppress FRDA Phenotypes in a Drosophila Model of the Disease. PLoS One. 2016; 11(7):e0159209.
    View in: PubMed
    Score: 0.015
  20. Uncoupling neuronal death and dysfunction in Drosophila models of neurodegenerative disease. Acta Neuropathol Commun. 2016 06 23; 4(1):62.
    View in: PubMed
    Score: 0.015
  21. TORC1 Inhibition by Rapamycin Promotes Antioxidant Defences in a Drosophila Model of Friedreich's Ataxia. PLoS One. 2015; 10(7):e0132376.
    View in: PubMed
    Score: 0.014
  22. A striatal-enriched intronic GPCR modulates huntingtin levels and toxicity. Elife. 2015 Mar 04; 4.
    View in: PubMed
    Score: 0.013
  23. 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: 0.013
  24. 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: 0.012
  25. 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: 0.012
  26. Tau loss attenuates neuronal network hyperexcitability in mouse and Drosophila genetic models of epilepsy. J Neurosci. 2013 Jan 23; 33(4):1651-9.
    View in: PubMed
    Score: 0.012
  27. 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: 0.011
  28. 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: 0.010
  29. The Drosophila FMRP and LARK RNA-binding proteins function together to regulate eye development and circadian behavior. J Neurosci. 2008 Oct 08; 28(41):10200-5.
    View in: PubMed
    Score: 0.009
  30. 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: 0.008
  31. Argonaute-2-dependent rescue of a Drosophila model of FXTAS by FRAXE premutation repeat. Hum Mol Genet. 2007 Oct 01; 16(19):2326-32.
    View in: PubMed
    Score: 0.008
  32. MBNL1 and CUGBP1 modify expanded CUG-induced toxicity in a Drosophila model of myotonic dystrophy type 1. Hum Mol Genet. 2006 Jul 01; 15(13):2138-45.
    View in: PubMed
    Score: 0.007
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.