Results 91 to 100 of about 23,657 (257)

Endothelial YAP Signaling Promotes Blood‐Spinal Cord Barrier Repair in Mice After Spinal Cord Injury

open access: yesAdvanced Science, EarlyView.
Endothelial YAP is required for blood‐spinal cord barrier repair after spinal cord injury. YAP‐dependent vascular repair is associated with ANGPT1/PI3K/AKT signaling in vivo and may involve endothelial‐pericyte paracrine interactions. By supporting vascular remodeling, tight junction restoration, restored pericyte coverage, and astrocyte‐vascular ...
Jiawei Wang   +14 more
wiley   +1 more source

Hydrocephalus induces dynamic spatiotemporal regulation of aquaporin-4 expression in the rat brain

open access: yesCerebrospinal Fluid Research, 2010
Background The water channel protein aquaporin-4 (AQP4) is reported to be of possible major importance for accessory cerebrospinal fluid (CSF) circulation pathways.
Praetorius Jeppe   +5 more
doaj   +1 more source

Update on the intriguing roles of AQP4 expression and redistribution in the progression and treatment of glioma

open access: yesAnnals of Medicine
Aquaporin 4 (AQP4) is abundant in the human brain and has an important role in brain homeostasis and diseases. AQP4 expression has been found to be associated with glioma malignancies.
Yu-Long Lan, Shuang Zou, Ruoli Chen
doaj   +1 more source

AQP4 autoantibodies in patients with idiopathic normal pressure hydrocephalus

open access: yes, 2020
Idiopathic normal pressure hydrocephalus (iNPH) is a common neurological disorder with unknown etiology. A selective depletion of aquaporin 4 (AQP4) has been shown in iNPH patients.
Claudio P.   +11 more
core   +1 more source

AQP4 NMD screen results.

open access: yes, 2021
Ranking, average log2 enrichments and false discovery rates for each gene in the AQP4 NMD screen, as computed by MAGeCK. (TXT)
Rachel Green (2365774)   +4 more
core   +1 more source

Clearance of activity-evoked K+ transients and associated glia cell swelling occur independently of AQP4:A study with an isoform-selective AQP4 inhibitor [PDF]

open access: yes, 2020
The mammalian brain consists of 80% water, which is continuously shifted between different compartments and cellular structures by mechanisms that are, to a large extent, unresolved.
Khandelia, Himanshu   +12 more
core   +1 more source

Effects of erythropoietin and methylprednisolone on AQP4 expression in astrocytes

open access: yesMolecular Medicine Reports, 2017
Methylprednisolone sodium succinate (MPSS) has been suggested as a treatment for spinal cord injury (SCI), but its use has been limited due to its adverse effects. Erythropoietin (EPO) has been suggested as a promising candidate for limiting SCI in mammals.
Wang, Changchao   +3 more
openaire   +3 more sources

TAB2 Causes Neuronal Damage by Aggravating Microglia‐Mediated Neuroinflammation in Parkinson's Disease

open access: yesAdvanced Science, EarlyView.
In microglia, STAT3 upregulates TAB2, which promotes NF‐κB activation through its NZF domain‐mediated recognition of K63‐linked ubiquitin chains, leading to inflammatory cytokine release and subsequent neuronal injury. Lumacaftor suppresses TAB2 expression and directly binds the TAB2‐NZF domain to interrupt K63 ubiquitin recognition, thereby blocking ...
Yanhao Zhao   +12 more
wiley   +1 more source

Nissl’s staining of AQP4+/+ and AQP4−/− mice.

open access: yes, 2013
Injection of rhVEGF165 intracerebroventricularly had no effect on Nissl’s staining in normal mice. At the three time points, marked neuron loss perihemotoma were found in AQP4−/− mice when compared to AQP4+/+ mice.
Yuping Tang (249674)   +2 more
core   +1 more source

TH/TRs–COL11A2 Axis Mediates Loss of a Differentiated Astrocyte State in Hypogyrified Brains

open access: yesAdvanced Science, EarlyView.
Using a gyrencephalic congenital hypothyroidism pig model, this study reveals cerebral atrophy and cortical hypogyrification. Single‐cell sequencing identifies astrocytes as major TH‐responsive cells, with the COL11A2‐enriched Astro‐2 state nearly absent.
Ying Zhang   +14 more
wiley   +1 more source

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