The PP2A-Aβ Gene is Regulated by Multiple Transcriptional Factors Including Ets-1, SP1/SP3, and RXRα /β

Liu, J.; Ji, Wei; Sun, Shuming; Zhang, L.; Chen, H. G.; Mao, Ying; Liu, L.; Zhang, X.; Gong, Lili; Deng, Mi; Chen, L.; Han, Wen; Chen, P. C.; Hu, Wenfeng; Hu, Xiao; Woodward, Zachary; Liu, W. B.; Xiao, Yamei; Liang, Shu‐Yuan; Liu, Y.; Liu, Shao Jun; Li, David Wan Cheng

doi:10.2174/156652412802480916

Cited by 62 publications

(80 citation statements)

References 49 publications

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“…These techniques can be used to create an artificial gauge potential that mimics the vector potential arising from the spin-orbit coupling (SOC), i.e., the interaction that couples the spin and momentum degrees of freedom [8,[11][12][13][14][15][16][17]. A special case of SOC is the RashbaDresselhaus (RD) coupling which is actively studied due to its relevance in spintronics [18][19][20].…”

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confidence: 99%

Stationary states of trapped spin-orbit-coupled Bose-Einstein condensates

Ruokokoski¹,

Huhtamäki²,

Möttönen³

2012

Phys. Rev. A

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We numerically investigate low-energy stationary states of pseudospin-1 Bose-Einstein condensates in the presence of Rashba-Dresselhaus-type spin-orbit coupling. We show that for experimentally feasible parameters and strong spin-orbit coupling, the ground state is a square vortex lattice irrespective of the nature of the spin-dependent interactions. For weak spin-orbit coupling, the lowest-energy state may host a single vortex. Furthermore, we analytically derive constraints that explain why certain stationary states do not emerge as ground states. Importantly, we show that the distinct stationary states can be observed experimentally by standard time-of-flight spinindependent absorption imaging.

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mentioning

confidence: 99%

Stationary states of trapped spin-orbit-coupled Bose-Einstein condensates

Ruokokoski¹,

Huhtamäki²,

Möttönen³

2012

Phys. Rev. A

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“…The time spent in the target quadrant on day 5 was also markedly longer in sham group at each time point. As synaptic plasticity is the neurobiological basis of cognitive function, [ 26 ] we then detected the expression of hippocampal synapse‐related proteins, including synaptophysin (Syp), postsynaptic density protein‐95 (Psd‐95), growth associated protein (Gap‐43), and synapsin IIa (Syn‐IIa) in VD and sham group. As shown in Figure S1b (Supporting Information), the expression levels of Syp, Psd‐95, Gap43, and Syn‐IIa in VD group gradually decreased from 0.5 to 8 months, and were much lower than those in sham group at 1, 2, 4, and 8 months respectively.…”

Section: Resultsmentioning

confidence: 99%

ESC‐sEVs Rejuvenate Senescent Hippocampal NSCs by Activating Lysosomes to Improve Cognitive Dysfunction in Vascular Dementia

Xia

Zhang

et al. 2020

Advanced Science

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Vascular dementia (VD) is one of the most common types of dementia, however, the intrinsic mechanism is unclear and there is still lack of effective medications. In this study, the VD rats exhibit a progressive cognitive impairment, as well as a time‐related increasing in hippocampal neural stem cells (H‐NSCs) senescence, lost and neurogenesis decline. Then, embryonic stem cell‐derived small extracellular vesicles (ESC‐sEVs) are intravenously injected into VD rats. ESC‐sEVs treatment significantly alleviates H‐NSCs senescence, recovers compromised proliferation and neuron differentiation capacity, and reverses cognitive impairment. By microarray analysis and RT‐qPCR it is identified that several miRNAs including miR‐17‐5p, miR‐18a‐5p, miR‐21‐5p, miR‐29a‐3p, and let‐7a‐5p, that can inhibit mTORC1 activation, exist in ESC‐sEVs. ESC‐sEVs rejuvenate H‐NSCs senescence partly by transferring these miRNAs to inhibit mTORC1 activation, promote transcription factor EB (TFEB) nuclear translocation and lysosome resumption. Taken together, these data indicate that H‐NSCs senescence cause cell depletion, neurogenesis reduction, and cognitive impairment in VD. ESC‐sEVs treatment ameliorates H‐NSCs senescence by inhibiting mTORC1 activation, and promoting TFEB nuclear translocation and lysosome resumption, thereby reversing senescence‐related neurogenesis dysfunction and cognitive impairment in VD. The application of ESC‐sEVs may be a novel cell‐free therapeutic tool for patients with VD, as well as other aging‐related diseases.

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“…Cell Lines-A clonal CHO cell line stably expressing the FLAG-hKOPR was generated previously (30,31), and the B max value of FLAG-hKOPR was ϳ1.9 pmol/mg of protein (32). Two clonal Neuro 2A cell lines expressing FLAG-hKOPR or 3HA-hKOPR were similarly established expressing ϳ1 pmol/mg protein of hKOPR.…”

Section: Methodsmentioning

confidence: 99%

Effects of C-terminal Modifications of GEC1 Protein and γ-Aminobutyric Acid Type A (GABAA) Receptor-associated Protein (GABARAP), Two Microtubule-associated Proteins, on κ Opioid Receptor Expression

Chen

Wang

Huang

et al. 2011

Journal of Biological Chemistry

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We demonstrated previously that GEC1, a member of the microtubule-associated protein (MAP) family, bound to the human opioid receptor (hKOPR) and promoted hKOPR cell surface expression by facilitating its trafficking along the secretory pathway. GABA A receptor-associated protein (GABARAP), a GEC1 analog, also enhanced KOPR expression, but to a lesser extent. The MAP family proteins undergo cleavage of their C-terminal residue(s), and the exposed conserved glycine forms conjugates with phosphatidylethanolamine, which associate with membranes. Here, we examined whether such modifications were required for GEC1 and GABARAP to enhance hKOPR expression. When transiently transfected into CHO or Neuro2A cells, GEC1 and GABARAP were cleaved at the C termini. G116A mutation alone or combined with deletion of Lys 117 in GEC1 (GEC1-A) or Leu 117 in GABARAP (GABARAP-A) blocked their C-terminal cleavage, indicating that the conserved Gly 116 is necessary for C-terminal modification. The two GEC1 mutants enhanced hKOPR expression to similar extents as the wildtype GEC1; however, the two GABARAP mutants did not. Immunofluorescence studies showed that HA-GEC1, HA-GEC1-A, and HA-GABARAP were distributed in a punctate manner and co-localized with KOPR-EGFP in the Golgi apparatus, whereas HA-GABARAP-A did not. Pulldown assay of GST-KOPR-C-tail with HA-GEC1 or HA-GABARAP revealed that GEC1 had stronger association with KOPR-Ctail than GABARAP. These results suggest that because of its stronger binding for hKOPR, GEC1 is able to be recruited by hKOPR sufficiently without membrane association via its C-terminal modification; however, due to its weaker affinity for the hKOPR, GABARAP appears to require C-terminal modifications to enhance KOPR expression. opioid receptor (KOPR) 2 is one of the three major types of opioid receptors mediating the effects of opioid drugs and endogenous peptides. The effects of KOPR activation in vivo include anti-nociception (especially for visceral chemical pain), anti-pruritic, water diuresis, and psychotomimetic effects (1). The KOPR agonist nalfurafine (TRK-820) is used clinically in Japan for the treatment of uremic pruritus in kidney dialysis patients (2). KOPR antagonists may be useful for curbing cocaine craving and as anti-anxiety drugs (3, 4). In addition, it has been proposed that KOPR agonists may be useful in treating mania, as antagonists as anti-depressants, and as partial agonists for the management of bipolar disorder (5).We have demonstrated that the protein glandular epithelial cell 1 (GEC1) interacts directly with the C-terminal domain of the KOPR by hydrophobic interactions (6, 7). The interaction increases cell surface expression of the KOPR by enhancing the conversion of the glycosylated intermediates to fully glycosylated forms of the receptor, indicating facilitation of trafficking from the endoplasmic reticulum to Golgi to plasma membranes (7).GEC1 was first cloned as an early estrogen-induced mRNA from guinea pig endometrial glandular epithelial cells (8). Its deduced amino a...

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The PP2A-Aβ Gene is Regulated by Multiple Transcriptional Factors Including Ets-1, SP1/SP3, and RXRα /β

Cited by 62 publications

References 49 publications

Stationary states of trapped spin-orbit-coupled Bose-Einstein condensates

Stationary states of trapped spin-orbit-coupled Bose-Einstein condensates

ESC‐sEVs Rejuvenate Senescent Hippocampal NSCs by Activating Lysosomes to Improve Cognitive Dysfunction in Vascular Dementia

Effects of C-terminal Modifications of GEC1 Protein and γ-Aminobutyric Acid Type A (GABAA) Receptor-associated Protein (GABARAP), Two Microtubule-associated Proteins, on κ Opioid Receptor Expression

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