Results 211 to 220 of about 104,244 (349)

LncRNA THUMPD3‐AS1 Regulates Behavioral and Synaptic Structural Abnormalities in Schizophrenia via miR‐485‐5p and ARHGAP8

open access: yesAdvanced Science, EarlyView.
Schizophrenia (SCZ) is linked to synaptic structural deficits driven by dysregulated noncoding RNAs. Using the novel ceRNAxis pipeline, THUMPD3‐AS1/miR‐485‐5p/ARHGAP8 is identified as a key regulator of actin cytoskeletal remodeling through noncanonical RhoB/C‐ROCK2 signaling. Modulating this axis ameliorates SCZ‐like phenotypes in mice and aligns with
Xiaojuan Gong   +9 more
wiley   +1 more source

Mex3a-dependent post-transcriptional silencing ensures olfactory receptor diversity and axon guidance specificity. [PDF]

open access: yesCell Rep
Duffié R   +16 more
europepmc   +1 more source

Axon Guidance Molecules in the Islets of Langerhans. [PDF]

open access: yesFront Endocrinol (Lausanne), 2022
Waters BJ, Blum B.
europepmc   +1 more source

Discovery of a Novel and Potent Kir4.1 Inhibitor as a Safe and Rapid‐Onset Antidepressant Agent in Mice

open access: yesAdvanced Science, EarlyView.
The preferred derivative JX3212 demonstrates strong inhibitory activity against Kir4.1 with favorable druggability and shows significant antidepressant efficacy in vivo. Abstract Major depressive disorder is a serious psychiatric disorder for which novel and fast‐acting antidepressants are required.
Sisi Wang   +15 more
wiley   +1 more source

Axon Guidance Molecules Guiding Neuroinflammation

open access: diamond, 2019
Won Suk Lee   +3 more
openalex   +2 more sources

Stress‐Induced Activation of Prolactin‐NR4A1‐Midkine Axis Exacerbates Skin Inflammation

open access: yesAdvanced Science, EarlyView.
Chronic psychological stress activates prolactin signaling to reprogram dermal fibroblasts into APCDD1+ inflammatory effectors via NR4A1, driving midkine secretion. This paracrine hub amplifies keratinocyte proliferation and immune recruitment, thus exacerbating skin inflammation.
Zhiguo Li   +18 more
wiley   +1 more source

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