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#35045339   2022/01/12 To Up

Social touch-like tactile stimulation activates a tachykinin 1-oxytocin pathway to promote social interactions.

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Hang Yu, Wanying Miao, En Ji, Shajin Huang, Sen Jin, Xutao Zhu, Ming-Zhe Liu, Yan-Gang Sun, Fuqiang Xu, Xiang Yu

2929 related Products with: Social touch-like tactile stimulation activates a tachykinin 1-oxytocin pathway to promote social interactions.

1 kit(96 Wells)200 ug2 Pieces/Box1 module0.1 mg1 module100 µg10 1 mg2 modules

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#35045338   2022/01/13 To Up

Acute restraint stress redirects prefrontal cortex circuit function through mGlu receptor plasticity on somatostatin-expressing interneurons.

Inhibitory interneurons orchestrate prefrontal cortex (PFC) activity, but we have a limited understanding of the molecular and experience-dependent mechanisms that regulate synaptic plasticity across PFC microcircuits. We discovered that mGlu receptor activation facilitates long-term potentiation at synapses from the basolateral amygdala (BLA) onto somatostatin-expressing interneurons (SST-INs) in mice. This plasticity appeared to be recruited during acute restraint stress, which induced intracellular calcium mobilization within SST-INs and rapidly potentiated postsynaptic strength onto SST-INs. Restraint stress and mGlu receptor activation each augmented BLA recruitment of SST-IN phasic feedforward inhibition, shunting information from other excitatory inputs, including the mediodorsal thalamus. Finally, studies using cell-type-specific mGlu receptor knockout mice revealed that mGlu receptor function in SST-expressing cells is necessary for restraint stress-induced changes to PFC physiology and related behaviors. These findings provide new insights into interneuron-specific synaptic plasticity mechanisms and suggest that SST-IN microcircuits may be promising targets for treating stress-induced psychiatric diseases.
Max E Joffe, James Maksymetz, Joseph R Luschinger, Shalini Dogra, Anthony S Ferranti, Deborah J Luessen, Isabel M Gallinger, Zixiu Xiang, Hannah Branthwaite, Patrick R Melugin, Kellie M Williford, Samuel W Centanni, Brenda C Shields, Craig W Lindsley, Erin S Calipari, Cody A Siciliano, Colleen M Niswender, Michael R Tadross, Danny G Winder, P Jeffrey Conn

1572 related Products with: Acute restraint stress redirects prefrontal cortex circuit function through mGlu receptor plasticity on somatostatin-expressing interneurons.

100ug Lyophilized96T1x107 IFU/ml x 200ul100ug200ul2 Pieces/Box100ug100ug Lyophilized100 μgUp to 200 ml cultures50ug 100ul

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#35045328   2022/01/16 To Up

Co-administration of rotavirus nanospheres VP6 and NSP4 proteins enhanced the anti-NSP4 humoral responses in immunized mice.

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Atefeh Afchangi, Somayeh Jalilvand, Arash Arashkia, Tayebeh Latifi, Mohammad Farahmand, Maryam Mashhadi Abolghasem Shirazi, Seyed Dawood Mousavi Nasab, Sayed Mahdi Marashi, Farzin Roohvand, Zabihollah Shoja

1738 related Products with: Co-administration of rotavirus nanospheres VP6 and NSP4 proteins enhanced the anti-NSP4 humoral responses in immunized mice.

25mg1mg100 μg1 mg100 μg100ug Lyophilized100ug

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#35045313   2022/01/16 To Up

CCN2 participates in overload-induced skeletal muscle hypertrophy.

The regulation of skeletal muscle growth following pro-hypertrophic stimuli requires a coordinated response by different cell types that leads to extracellular matrix (ECM) remodeling and increases in muscle cross-sectional area. Indeed, matricellular proteins serve a key role as communication vehicles that facilitate the propagation of signaling stimuli required for muscle adaptation to environmental challenges. We found that the matricellular protein cellular communication network factor 2 (CCN2), also known as connective tissue growth factor (CTGF), is induced during a time course of overload-driven skeletal muscle hypertrophy in mice. To elucidate the role of CCN2 in mediating the hypertrophic response, we utilized genetically engineered mouse models for myofiber-specific CCN2 gain- and loss-of-function and then examined their response to mechanical stimuli through muscle overload. Interestingly, myofiber-specific deletion of CCN2 blunted muscle's hypertrophic response to overload without interfering with ECM deposition. On the other hand, when in excess through transgenic CCN2 overexpression, CCN2 was efficient in promoting overload-induced aberrant ECM accumulation without affecting myofiber growth. Altogether, our genetic approaches highlighted independent ECM and myofiber stress adaptation responses, and positioned CCN2 as a central mediator of both. Mechanistically, CCN2 acts by regulating focal adhesion kinase (FAK) mediated transduction of overload-induced extracellular signals, including interleukin 6 (IL6), and their regulatory impact on global protein synthesis in skeletal muscle. Overall, our study highlights the contribution of muscle-derived extracellular matrix factor CCN2 for proper hypertrophic muscle growth.
Jennifer M Petrosino, Jacob Z Longenecker, Colin D Angel, Scott A Hinger, Colton R Martens, Federica Accornero

1544 related Products with: CCN2 participates in overload-induced skeletal muscle hypertrophy.

2ug100ug100 ul96 assays96 wells200ul400 ug10 mg100 ul400 ug96T5 mg

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#35045306   // To Up

Seasonal shift of the gut microbiome synchronizes host peripheral circadian rhythm for physiological adaptation to a low-fat diet in the giant panda.

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Guangping Huang, Le Wang, Jian Li, Rong Hou, Meng Wang, Zhilin Wang, Qingyue Qu, Wenliang Zhou, Yonggang Nie, Yibo Hu, Yingjie Ma, Li Yan, Hong Wei, Fuwen Wei

2627 related Products with: Seasonal shift of the gut microbiome synchronizes host peripheral circadian rhythm for physiological adaptation to a low-fat diet in the giant panda.

1100 ul100 ml0.1ml

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#35045305   // To Up

CXCR3 regulates stem and proliferative CD8+ T cells during chronic infection by promoting interactions with DCs in splenic bridging channels.

Production of effector CD8+ T cells during persistent infection requires a stable pool of stem-like cells that can give rise to effector cells via a proliferative intermediate population. In infection models marked by T cell exhaustion, this process can be transiently induced by checkpoint blockade but occurs spontaneously in mice chronically infected with the protozoan intracellular parasite Toxoplasma gondii. We observe distinct locations for parasite-specific T cell subsets, implying a link between differentiation and anatomical niches in the spleen. Loss of the chemokine receptor CXCR3 on T cells does not prevent white pulp-to-red pulp migration but reduces interactions with CXCR3 ligand-producing dendritic cells (DCs) and impairs memory-to-intermediate transition, leading to a buildup of memory T cells in the red pulp. Thus, CXCR3 increases T cell exposure to differentiation-inducing signals during red pulp migration, providing a dynamic mechanism for modulating effector differentiation in response to environmental signals.
Derek J Bangs, Alexandra Tsitsiklis, Zoë Steier, Shiao Wei Chan, James Kaminski, Aaron Streets, Nir Yosef, Ellen A Robey

1698 related Products with: CXCR3 regulates stem and proliferative CD8+ T cells during chronic infection by promoting interactions with DCs in splenic bridging channels.

96 tests1 mg96 tests10 ug96 tests96 tests

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