Maureen H. Richards
Rush University Medical Center
15 Papers
99 Citations
Maureen H. Richards is an academic researcher from Rush University Medical Center. The author has contributed to research in topics: T cell & CD8. The author has an hindex of 12, co-authored 15 publications. Previous affiliations of Maureen H. Richards include Northwestern University.
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Papers
HIV and drug abuse mediate astrocyte senescence in a β-catenin-dependent manner leading to neuronal toxicity.
Chunjiang Yu,Srinivas D. Narasipura,Maureen H. Richards,Xiu-Ti Hu,Bryan K. Yamamoto,Lena Al-Harthi +5 more
TL;DR: It is shown that β‐catenin, a pro‐survival/proliferation transcriptional co‐activator, is downregulated by HIV and meth in human astrocytes and this downregulation promotesAstrocyte senescence while induction of β‐ catenin blocks HIV‐ and meth‐mediated astro Cytokine Senescence.
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A critical role for virus-specific CD8(+) CTLs in protection from Theiler's virus-induced demyelination in disease-susceptible SJL mice.
TL;DR: O adoptive transfer of activated CD8(+) VP3(159)(-)(166)-specific T cell blasts shortly after TMEV infection to boost the early anti-viral response leads to clearance of CNS virus and protection from subsequent TMEv-IDD.
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Porcupine is not required for the production of the majority of Wnts from primary human astrocytes and CD8+ T cells.
TL;DR: The data indicate that porcupine-mediated production of Wnts is context dependent and is not required for all WNTs production, suggesting that alternative mechanisms exist for Wnt’s production.
HIV and drug abuse mediate astrocyte senescence in a β‐catenin‐dependent manner leading to neuronal toxicity
Chunjiang Yu,Srinivas D. Narasipura,Maureen H. Richards,Xiu-Ti Hu,Bryan K. Yamamoto,Lena Al-Harthi +5 more
- 01 Oct 2017
TL;DR: In this article, the authors evaluated the impact of HIV and meth on astrocyte senescence using in vitro and several animal models, and for the first time, they demonstrated that the β-catenin pathway is a potential therapeutic target to overcome the effect of HIV-associated neurocognitive disorders.
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Human FasL gene is a target of β-catenin/T-cell factor pathway and complex FasL haplotypes alter promoter functions.
Jianming Wu,Maureen H. Richards,Jinhai Huang,Lena Al-Harthi,Xiulong Xu,Rui Lin,Fenglong Xie,Andrew W. Gibson,Jeffrey C. Edberg,Robert P. Kimberly +9 more
TL;DR: The data suggest that β-catenin may be involved in FasL gene regulation and that FasL expression is influenced by FasL SNP haplotypes, which may have significant implications in immune response and tumorigenesis.