Results 131 to 140 of about 821,290 (231)

NSD2 Coordinates the Neurogenic‐to‐Gliogenic Transition via H3K36me2‐Dependent Activation of the EGFR‐ERK Pathway

open access: yesAdvanced Science, EarlyView.
NSD2 coordinates the neurogenic‐to‐gliogenic transition in the developing neocortex through H3K36me2‐dependent activation of EGFR–ERK signaling. Loss of NSD2 disrupts astroglial and oligodendroglial development, whereas ERK activation rescues gliogenic defects in vitro and in vivo.
Hanxue Chen   +7 more
wiley   +1 more source

UvA-DARE (Digital Academic Repository) Inactivating mutations in the gene for thyroid oxidase 2 (THOX2) and congenital hypothyroidism Link to publication Citation for published version (APA): INACTIVATING MUTATIONS IN THE GENE FOR THYROID OXIDASE 2 ( THOX

open access: yes, 2020
. Inactivating mutations in the gene for thyroid oxidase 2 (THOX2) and congenital hypothyroidism. The New England journal of medicine, 347(2), 95-102.
Mutations, Congenital
core  

Aberrant GRP78 Phase Transition Sustains Endothelial IRE1α Signaling and Drives Blood–Brain Barrier Failure in Cerebral Amyloid Angiopathy

open access: yesAdvanced Science, EarlyView.
Vascular Aβ40 corrupts GRP78 phase behavior in brain endothelial cells, sustaining IRE1α–TRAF2–JNK signaling and driving apoptosis, tight junction loss, and blood–brain barrier failure in cerebral amyloid angiopathy. Pharmacological IRE1α inhibition restores vascular integrity, reduces leakage, and improves functional outcomes, revealing a targetable ...
Honglin Zheng   +19 more
wiley   +1 more source

A Blood‐Derived Factor Rescues ALS: Platelet Factor 4 Activates OPTN‐Dependent Autophagy to Clear SOD1 Aggregates Independently of PINK1

open access: yesAdvanced Science, EarlyView.
Systemic platelet factor 4 (PF4) is significantly depleted in amyotrophic lateral sclerosis (ALS). Peripheral PF4 replenishment restores central proteostasis by driving OPTN‐dependent, PINK1‐independent selective autophagy in motor neurons. This intervention effectively clears toxic SOD1 aggregates, blunts glial activation, and preserves neuromuscular ...
Qingjian Xie   +12 more
wiley   +1 more source

Compensatory evolution of chromosomes and plasmids counteracts the plasmid fitness cost

open access: yesEcology and Evolution
Plasmids incur a fitness cost that has the potential to restrict the dissemination of resistance in bacterial pathogens. However, bacteria can overcome this disadvantage by compensatory evolution to maintain their resistance.
Ziyi Liu   +3 more
doaj   +1 more source

Deep phylogeny of cancer drivers and compensatory mutations. [PDF]

open access: yesCommun Biol, 2020
Rochman ND, Wolf YI, Koonin EV.
europepmc   +1 more source

Targeting the KCNC3‐Dependent Anterior Insular‐Lateral Orbitofrontal Cortex Glutamatergic Circuit Attenuates Post‐Traumatic Anxiety

open access: yesAdvanced Science, EarlyView.
Frontal lobe traumatic brain injury is associated with hyperactivity of an insular–orbitofrontal circuit in both patients and mice. By combination of integrating functional imaging, cell‐type–specific circuit manipulation, single‐cell transcriptomics, and whole‐cell recordings, this work identifies the downregulation of the potassium channel KCNC3 in ...
Meng‐Ge Li   +10 more
wiley   +1 more source

Genetic Ablation and Multi‐Omics Profiling Reveal CEP55 as a Key Driver of Tumorigenesis in Diverse Cancer Models

open access: yesAdvanced Science, EarlyView.
Genetic ablation of Cep55 in Pten‐deficient mouse models delays tumorigenesis. Integrated multi‐omics analyses (proteomics, phosphoproteomics, and spatial transcriptomics) reveal that CEP55 regulates oncogenic signaling (RAS/ERK, PI3K/AKT), integrin/FAK‐mediated adhesion, extracellular matrix (ECM) remodeling, and endocytosis.
Behnam Rashidieh   +22 more
wiley   +1 more source

Selection Intensity Against Deleterious Mutations in RNA Secondary Structures and Rate of Compensatory Nucleotide Substitutions

open access: yes, 2001
A two-locus model of reversible mutations with compensatory fitness interactions is presented; single mutations are assumed to be deleterious but neutral in appropriate combinations. The expectation of the time of compensatory nucleotide substitutions is
印南, 秀樹   +2 more
core  

EDNRA Forms a Positive Feedback Loop with the Hippo/YAP Axis to Drive Triple‐Negative Breast Cancer Progression

open access: yesAdvanced Science, EarlyView.
Endothelin receptor type A (EDNRA) and the Hippo/YAP pathway form a self‐reinforcing loop that sustains triple‐negative breast cancer. EDNRA activates YAP through Gαq/11–Rho/ROCK–LATS signaling, while YAP/TEAD4 reciprocally drives EDNRA transcription.
Zehao Hong   +10 more
wiley   +1 more source

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