Connection

ISMAEL AL-RAMAHI to Humans

This is a "connection" page, showing publications ISMAEL AL-RAMAHI has written about Humans.
Connection Strength

0.164
  1. 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
  2. Inhibition of PIP4K? ameliorates the pathological effects of mutant huntingtin protein. Elife. 2017 12 26; 6.
    View in: PubMed
    Score: 0.016
  3. 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: 0.007
  4. 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
  5. TMEM106B coding variant is protective and deletion detrimental in a mouse model of tauopathy. Acta Neuropathol. 2024 03 25; 147(1):61.
    View in: PubMed
    Score: 0.006
  6. Tau polarizes an aging transcriptional signature to excitatory neurons and glia. Elife. 2023 May 23; 12.
    View in: PubMed
    Score: 0.006
  7. Functional screening of lysosomal storage disorder genes identifies modifiers of alpha-synuclein neurotoxicity. PLoS Genet. 2023 05; 19(5):e1010760.
    View in: PubMed
    Score: 0.006
  8. Functional variants identify sex-specific genes and pathways in Alzheimer's Disease. Nat Commun. 2023 05 13; 14(1):2765.
    View in: PubMed
    Score: 0.006
  9. Evolutionarily conserved regulators of tau identify targets for new therapies. Neuron. 2023 03 15; 111(6):824-838.e7.
    View in: PubMed
    Score: 0.006
  10. Cross-species genetic screens identify transglutaminase 5 as a regulator of polyglutamine-expanded ataxin-1. J Clin Invest. 2022 05 02; 132(9).
    View in: PubMed
    Score: 0.006
  11. Inhibition of HIPK3 by AST487 Ameliorates Mutant HTT-Induced Neurotoxicity and Apoptosis via Enhanced Autophagy. Neurosci Bull. 2022 Jan; 38(1):99-103.
    View in: PubMed
    Score: 0.005
  12. 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: 0.005
  13. Downregulation of glial genes involved in synaptic function mitigates Huntington's disease pathogenesis. Elife. 2021 04 19; 10.
    View in: PubMed
    Score: 0.005
  14. Dual targeting of brain region-specific kinases potentiates neurological rescue in Spinocerebellar ataxia type 1. EMBO J. 2021 04 01; 40(7):e106106.
    View in: PubMed
    Score: 0.005
  15. Harnessing the paradoxical phenotypes of APOE ?2 and APOE ?4 to identify genetic modifiers in Alzheimer's disease. Alzheimers Dement. 2021 05; 17(5):831-846.
    View in: PubMed
    Score: 0.005
  16. 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: 0.005
  17. A Druggable Genome Screen Identifies Modifiers of a-Synuclein Levels via a Tiered Cross-Species Validation Approach. J Neurosci. 2018 10 24; 38(43):9286-9301.
    View in: PubMed
    Score: 0.004
  18. TRIM28 regulates the nuclear accumulation and toxicity of both alpha-synuclein and tau. Elife. 2016 10 25; 5.
    View in: PubMed
    Score: 0.004
  19. 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: 0.004
  20. Metal Homeostasis Regulators Suppress FRDA Phenotypes in a Drosophila Model of the Disease. PLoS One. 2016; 11(7):e0159209.
    View in: PubMed
    Score: 0.004
  21. 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: 0.003
  22. 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: 0.003
  23. A striatal-enriched intronic GPCR modulates huntingtin levels and toxicity. Elife. 2015 Mar 04; 4.
    View in: PubMed
    Score: 0.003
  24. 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: 0.003
  25. 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: 0.003
  26. Smaug/SAMD4A restores translational activity of CUGBP1 and suppresses CUG-induced myopathy. PLoS Genet. 2013 Apr; 9(4):e1003445.
    View in: PubMed
    Score: 0.003
  27. 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: 0.003
  28. 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: 0.003
  29. Network organization of the huntingtin proteomic interactome in mammalian brain. Neuron. 2012 Jul 12; 75(1):41-57.
    View in: PubMed
    Score: 0.003
  30. 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: 0.003
  31. 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: 0.002
  32. 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: 0.002
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.