Untargeted Metabolomics and Steroid Signatures in Urine of Male Pattern Baldness Patients after Finasteride Treatment for a Year

Autor: Yu Ra Lee, Eunju Im, Haksoon Kim, Bark Lynn Lew, Woo-Young Sim, Jeongae Lee, Han Bin Oh, Ki Jung Paeng, Jongki Hong, Bong Chul Chung

Publikováno v: Metabolites, Vol 10, Iss 4, p 131 (2020)

Male pattern baldness (MPB) has been associated with dihydrotestosterone (DHT) expression. Finasteride treats MPB by inhibiting 5-alpha reductase and blocking DHT production. In this study, we aimed to identify metabolic differences in urinary metabo

Externí odkaz: https://doaj.org/article/a5b7f138b4134b04905f482feed4aae9

Histone deacetylase 3 promotes RCAN1 stability and nuclear translocation.

Autor: Kyung Ah Han, Hye Seon Kang, Jee Won Lee, Lang Yoo, Eunju Im, Ahyoung Hong, Yun Ju Lee, Woo Hyun Shin, Kwang Chul Chung

Publikováno v: PLoS ONE, Vol 9, Iss 8, p e105416 (2014)

Regulator of calcineurin 1 (RCAN1; also referred as DSCR1 or MCIP1) is located in close proximity to a Down syndrome critical region of human chromosome 21. Although RCAN1 is an endogenous inhibitor of calcineurin signaling that controls lymphocyte a

Externí odkaz: https://doaj.org/article/d131da4e0fb6475eba02ccf3ae0d2db8

Faulty autolysosome acidification in Alzheimer’s disease mouse models induces autophagic build-up of Aβ in neurons, yielding senile plaques

Autor: Ju-Hyun Lee, Dun-Sheng Yang, Chris N. Goulbourne, Eunju Im, Philip Stavrides, Anna Pensalfini, Han Chan, Cedric Bouchet-Marquis, Cynthia Bleiwas, Martin J. Berg, Chunfeng Huo, James Peddy, Monika Pawlik, Efrat Levy, Mala Rao, Mathias Staufenbiel, Ralph A. Nixon

Publikováno v: Nature Neuroscience. 25:688-701

Autophagy is markedly impaired in Alzheimer’s disease (AD). Here we reveal unique autophagy dysregulation within neurons in five AD mouse models in vivo and identify its basis using a neuron-specific transgenic mRFP-eGFP-LC3 probe of autophagy and

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0c5bc48852728fc53fbe780572287d2d
https://doi.org/10.1038/s41593-022-01084-8

The three-dimensional landscape of cortical chromatin accessibility in Alzheimer’s disease

Autor: Jaroslav Bendl, Mads E. Hauberg, Kiran Girdhar, Eunju Im, James M. Vicari, Samir Rahman, Michael B. Fernando, Kayla G. Townsley, Pengfei Dong, Ruth Misir, Steven P. Kleopoulos, Sarah M. Reach, Pasha Apontes, Biao Zeng, Wen Zhang, Georgios Voloudakis, Kristen J. Brennand, Ralph A. Nixon, Vahram Haroutunian, Gabriel E. Hoffman, John F. Fullard, Panos Roussos

Publikováno v: Bendl, J, Hauberg, M E, Girdhar, K, Im, E, Vicari, J M, Rahman, S, Fernando, M B, Townsley, K G, Dong, P, Misir, R, Kleopoulos, S P, Reach, S M, Apontes, P, Zeng, B, Zhang, W, Voloudakis, G, Brennand, K J, Nixon, R A, Haroutunian, V, Hoffman, G E, Fullard, J F & Roussos, P 2022, ' The three-dimensional landscape of cortical chromatin accessibility in Alzheimer’s disease ', Nature Neuroscience, vol. 25, no. 10, pp. 1366-1378 . https://doi.org/10.1038/s41593-022-01166-7
Nat Neurosci

To characterize the dysregulation of chromatin accessibility in Alzheimer’s disease (AD), we generated 636 ATAC-seq libraries from neuronal and nonneuronal nuclei isolated from the superior temporal gyrus and entorhinal cortex of 153 AD cases and 5

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::50ed5dff7de685cf1d386373b8ad4009
https://pure.au.dk/portal/da/publications/the-threedimensional-landscape-of-cortical-chromatin-accessibility-in-alzheimers-disease(6777827c-e6bb-4e67-b387-dec7c9ba155f).html

Lysosomal dysfunction in Down Syndrome and Alzheimer mouse models is caused by selective v-ATPase inhibition by Tyr682phosphorylated APP βCTF

Autor: Eunju Im, Ying Jiang, Philip Stavrides, Sandipkumar Darji, Hediye Erdjument-Bromage, Thomas A. Neubert, Jun Yong Choi, Jerzy Wegiel, Ju-Hyun Lee, Ralph A. Nixon

Lysosome dysfunction arises early and propels Alzheimer’s Disease (AD). Herein, we show that amyloid precursor protein (APP), linked to early-onset AD in Down Syndrome (DS), acts directly via its β-C-terminal fragment (βCTF) to disrupt lysosomal

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::e98d3efd72620e8895fb69f4ded88179
https://doi.org/10.1101/2022.06.02.494546