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• W2745235335 endingPage "109" @default.
• W2745235335 startingPage "101" @default.
• W2745235335 abstract "Heat shock protein beta-1 (HSPB1), is a ubiquitously expressed, multifunctional protein chaperone. Mutations in HSPB1 result in the development of a late-onset, distal hereditary motor neuropathy type II (dHMN) and axonal Charcot-Marie Tooth disease with sensory involvement (CMT2F). The functional consequences of HSPB1 mutations associated with hereditary neuropathy are unknown. HSPB1 also displays neuroprotective properties in many neuronal disease models, including the motor neuron disease amyotrophic lateral sclerosis (ALS). HSPB1 is upregulated in SOD1-ALS animal models during disease progression, predominately in glial cells. Glial cells are known to contribute to motor neuron loss in ALS through a non-cell autonomous mechanism. In this study, we examined the non-cell autonomous role of wild type and mutant HSPB1 in an astrocyte-motor neuron co-culture model system of ALS. Astrocyte-specific overexpression of wild type HSPB1 was sufficient to attenuate SOD1(G93A) astrocyte-mediated toxicity in motor neurons, whereas, overexpression of mutHSPB1 failed to ameliorate motor neuron toxicity. Expression of a phosphomimetic HSPB1 mutant in SOD1(G93A) astrocytes also reduced toxicity to motor neurons, suggesting that phosphorylation may contribute to HSPB1 mediated-neuroprotection. These data provide evidence that astrocytic HSPB1 expression may play a central role in motor neuron health and maintenance." @default.
• W2745235335 created "2017-08-17" @default.
• W2745235335 creator A5007174970 @default.
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• W2745235335 creator A5086564788 @default.
• W2745235335 date "2017-11-01" @default.
• W2745235335 modified "2023-09-26" @default.
• W2745235335 title "HSPB1 mutations causing hereditary neuropathy in humans disrupt non-cell autonomous protection of motor neurons" @default.
• W2745235335 cites W1511318907 @default.
• W2745235335 cites W1680824007 @default.
• W2745235335 cites W1696695876 @default.
• W2745235335 cites W1944113437 @default.
• W2745235335 cites W1958033040 @default.
• W2745235335 cites W1965589408 @default.
• W2745235335 cites W1967411211 @default.
• W2745235335 cites W1969202288 @default.
• W2745235335 cites W1972380090 @default.
• W2745235335 cites W1974529717 @default.
• W2745235335 cites W1978522737 @default.
• W2745235335 cites W1978632856 @default.
• W2745235335 cites W1979480555 @default.
• W2745235335 cites W1985838757 @default.
• W2745235335 cites W1990078383 @default.
• W2745235335 cites W1993190166 @default.
• W2745235335 cites W1994350510 @default.
• W2745235335 cites W1994700524 @default.
• W2745235335 cites W1995885857 @default.
• W2745235335 cites W1996024251 @default.
• W2745235335 cites W1996437447 @default.
• W2745235335 cites W2000461947 @default.
• W2745235335 cites W2004747044 @default.
• W2745235335 cites W2011893442 @default.
• W2745235335 cites W2012851706 @default.
• W2745235335 cites W2017198566 @default.
• W2745235335 cites W2020481807 @default.
• W2745235335 cites W2022814422 @default.
• W2745235335 cites W2026955814 @default.
• W2745235335 cites W2027014645 @default.
• W2745235335 cites W2030428515 @default.
• W2745235335 cites W2030674861 @default.
• W2745235335 cites W2032415844 @default.
• W2745235335 cites W2041849406 @default.
• W2745235335 cites W2044659434 @default.
• W2745235335 cites W2046439284 @default.
• W2745235335 cites W2059355164 @default.
• W2745235335 cites W2060728994 @default.
• W2745235335 cites W2064620995 @default.
• W2745235335 cites W2069950833 @default.
• W2745235335 cites W2070154661 @default.
• W2745235335 cites W2070200157 @default.
• W2745235335 cites W2071296558 @default.
• W2745235335 cites W2073757903 @default.
• W2745235335 cites W2075382996 @default.
• W2745235335 cites W2076083579 @default.
• W2745235335 cites W2076363178 @default.
• W2745235335 cites W2077672936 @default.
• W2745235335 cites W2077831889 @default.
• W2745235335 cites W2083796374 @default.
• W2745235335 cites W2085434406 @default.
• W2745235335 cites W2088846224 @default.
• W2745235335 cites W2089144722 @default.
• W2745235335 cites W2096386031 @default.
• W2745235335 cites W2099671775 @default.
• W2745235335 cites W2101321540 @default.
• W2745235335 cites W2107975828 @default.
• W2745235335 cites W2110633413 @default.
• W2745235335 cites W2111692215 @default.
• W2745235335 cites W2117516401 @default.
• W2745235335 cites W2117998622 @default.
• W2745235335 cites W2121726351 @default.
• W2745235335 cites W2128352763 @default.
• W2745235335 cites W2133072585 @default.
• W2745235335 cites W2140834315 @default.
• W2745235335 cites W2141561409 @default.
• W2745235335 cites W2143609278 @default.
• W2745235335 cites W2148209200 @default.
• W2745235335 cites W2154549928 @default.
• W2745235335 cites W2154904733 @default.
• W2745235335 cites W2156588282 @default.
• W2745235335 cites W2156759248 @default.
• W2745235335 cites W2157894520 @default.
• W2745235335 cites W2164064654 @default.
• W2745235335 cites W2308848840 @default.
• W2745235335 cites W2340689227 @default.
• W2745235335 cites W2344042153 @default.
• W2745235335 cites W2360054760 @default.
• W2745235335 cites W2366800531 @default.
• W2745235335 cites W2412819794 @default.
• W2745235335 cites W2491299425 @default.
• W2745235335 cites W2513364739 @default.
• W2745235335 cites W2528482039 @default.
• W2745235335 doi "https://doi.org/10.1016/j.expneurol.2017.08.002" @default.

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