His primary areas of study are Genetics, Cell biology, Huntingtin, Polyglutamine tract and Neurodegeneration. His Cell biology study frequently links to related topics such as Ataxin 1. He works mostly in the field of Huntingtin, limiting it down to concerns involving Molecular biology and, occasionally, Gene expression, Tetratricopeptide, Chaperone and Nuclear protein.
He has included themes like Spinocerebellar Ataxia Type 1, Genetic screen and Protein–protein interaction in his Polyglutamine tract study. His Neurodegeneration study frequently intersects with other fields, such as Ubiquitin ligase. His Huntingtin Protein research includes themes of Cerebral cortex and Proteomics.
Juan Botas spends much of his time researching Cell biology, Genetics, Neurodegeneration, Huntingtin and Neuroscience. The concepts of his Cell biology study are interwoven with issues in Alpha-synuclein, Trinucleotide repeat expansion, Regulation of gene expression and Nuclear protein, Ataxin 1. The study incorporates disciplines such as Spinocerebellar Ataxia Type 1 and Spinocerebellar ataxia in addition to Ataxin 1.
His study in Neurodegeneration is interdisciplinary in nature, drawing from both Alzheimer's disease, Gene knockdown, Chaperone and Genetic screen. His Huntingtin study incorporates themes from Molecular biology, Gene expression and DNA damage. His study looks at the intersection of Neuroscience and topics like Disease with Computational biology.
His scientific interests lie mostly in Neurodegeneration, Spinocerebellar Ataxia Type 1, Ataxin 1, Cell biology and Disease. His Neurodegeneration study frequently draws parallels with other fields, such as Gene. His Spinocerebellar Ataxia Type 1 study combines topics from a wide range of disciplines, such as Kinase and Genetic screen.
His research on Cell biology often connects related topics like Huntingtin. His work is dedicated to discovering how Disease, Computational biology are connected with RNA interference, Druggability, Small hairpin RNA, Genome and Copy-number variation and other disciplines. His research investigates the connection with Apolipoprotein E and areas like Genetics which intersect with concerns in Evolutionary information.
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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)
Daniel J. Klionsky;Amal Kamal Abdel-Aziz;Sara Abdelfatah;Mahmoud Abdellatif.
Identification of genes that modify ataxin-1-induced neurodegeneration
Pedro Fernandez-Funez;Maria Laura Nino-Rosales;Beatrice De Gouyon;Wei Chi She.
Homeotic genes of the bithorax complex repress limb development in the abdomen of the Drosophila embryo through the target gene Distal-less
Gilles Vachon;Barbara Cohen;Christine Pfeifle;M.Elaine McGuffin.
Interaction of Akt-Phosphorylated Ataxin-1 with 14-3-3 Mediates Neurodegeneration in Spinocerebellar Ataxia Type 1
Hung Kai Chen;Hung Kai Chen;Pedro Fernandez-Funez;Summer F. Acevedo;Yung C. Lam.
Huntingtin interacting proteins are genetic modifiers of neurodegeneration.
Linda S. Kaltenbach;Eliana Romero;Robert R. Becklin;Rakesh Chettier.
PLOS Genetics (2007)
The DNA binding specificity of ultrabithorax is modulated by cooperative interactions with extradenticle, another homeoprotein
Siu-Kwong Chan;Leah Jaffe;Maria Capovilla;Juan Botas.
RNA-binding proteins hnRNP A2/B1 and CUGBP1 suppress fragile X CGG premutation repeat-induced neurodegeneration in a Drosophila model of FXTAS
Oyinkan A. Sofola;Peng Jin;Yunlong Qin;Ranhui Duan.
ATAXIN-1 Interacts with the Repressor Capicua in Its Native Complex to Cause SCA1 Neuropathology
Yung C. Lam;Aaron B. Bowman;Paymaan Jafar-Nejad;Janghoo Lim.
CHIP protects from the neurotoxicity of expanded and wild-type ataxin-1 and promotes their ubiquitination and degradation.
Ismael Al-Ramahi;Ismael Al-Ramahi;Yung C. Lam;Hung Kai Chen;Beatrice De Gouyon.
Journal of Biological Chemistry (2006)
Network Organization of the Huntingtin Proteomic Interactome in Mammalian Brain
Dyna I. Shirasaki;Dyna I. Shirasaki;Erin R. Greiner;Erin R. Greiner;Ismael Al-Ramahi;Michelle Gray;Michelle Gray.
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