Results 101 to 110 of about 1,397,252 (312)

The C‐terminal truncated splicing variant of NK1R negatively modulates substance P‐stimulated NK1R signaling

open access: yesFEBS Open Bio, EarlyView.
The neurokinin 1 receptor exists as full‐length (NK1L) and C‐terminally truncated (NK1S) splice variants. We show that NK1S heterodimerizes with NK1L, impairing Gαq coupling and Ca2+ mobilization while enhancing β‐arrestin1 recruitment. NK1S suppresses substance P‐driven gene expression and cell migration, revealing NK1S as an endogenous biased ...
Lan Phuong Nguyen   +8 more
wiley   +1 more source

Hsp27 upregulation and phosphorylation is required for injured sensory and motor neuron survival

open access: yes, 2002
Peripheral nerve transection results in the rapid death by apoptosis of neonatal but not adult sensory and motor neurons. We show that this is due to induction and phosphorylation in all adult axotomized neurons of the small heat shock protein Hsp27 and ...
Decosterd, I.   +7 more
core   +1 more source

MARK4 enhances stress granule formation under oxidative stress and increases tau accumulation

open access: yesFEBS Open Bio, EarlyView.
MARK4 (red dots) localizes to stress granules (orange dots) and promotes their formation under oxidative stress by modulating TIA1 (blue dots). MARK4 and TIA1 synergistically increase tau (purple) accumulation, and the reduction of the TIA1 ortholog suppresses neurodegeneration in a fly model.
Sho Nakajima   +8 more
wiley   +1 more source

Beta1 subunits enable fentanyl‐induced BK channel activation and opioid regulation of cerebral artery diameter

open access: yesFEBS Open Bio, EarlyView.
During the current opioid crisis, the majority of overdose deaths are attributed to ultra‐potent synthetic opioids, such as fentanyl. While fentanyl exerts its action via opioid receptors, we propose that potassium channels in the brain blood vessels may also sense fentanyl.
Shiwani Thapa   +4 more
wiley   +1 more source

MNX1 (motor neuron and pancreas homeobox 1) [PDF]

open access: yes, 2004
Review on MNX1 (motor neuron and pancreas homeobox 1), with data on DNA, on the protein encoded, and where the gene is ...
HB Beverloo   +3 more
core   +1 more source

Spliceosome integrity is defective in the motor neuron diseases ALS and SMA

open access: yesEMBO Molecular Medicine, 2013
Two motor neuron diseases, amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA), are caused by distinct genes involved in RNA metabolism, TDP‐43 and FUS/TLS, and SMN, respectively.
Hitomi Tsuiji   +11 more
doaj   +1 more source

Proteomics Approaches for Biomarker and Drug Target Discovery in ALS and FTD

open access: yesFrontiers in Neuroscience, 2019
Neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are increasing in prevalence but lack targeted therapeutics. Although the pathological mechanisms behind these diseases remain unclear, both ALS and
Thomas J. Hedl   +11 more
doaj   +1 more source

Dactolisib outperforms Rapamycin in potentiating apoptosis induced by XPO1, Bcl‐2 and Mcl‐1 blockade in preclinical glioblastoma models

open access: yesFEBS Open Bio, EarlyView.
The PAM pathway and its impact on cellular metabolism. Color‐coded key symbols represent Rapamycin (R, orange, targeting mTOR) and Dactolisib (D, green, targeting PI3K/mTOR), indicating their sites of action. Created with BioRenders.com. Glioblastoma resists therapy through interconnected survival programs.
Kai Zhao   +23 more
wiley   +1 more source

Identification and outcomes of clinical phenotypes in amyotrophic lateral sclerosis/motor neuron disease: Australian National Motor Neuron Disease observational cohort

open access: yes, 2016
Identification and outcomes of clinical phenotypes in amyotrophic lateral sclerosis/motor neuron disease: Australian National Motor Neuron Disease observational ...
P Talman (13420677)   +13 more
core  

Chronobiology of Cancer: How Aging Fuels Oncogenesis at the Molecular Level

open access: yesAging and Cancer, EarlyView.
This graphical abstract illustrates the key biological pathways linking aging with cancer development and progression. In the upper left, cumulative exposure to ultraviolet radiation, toxins, and reactive oxygen species (ROS) causes DNA damage and genomic instability, whereas age‐related decline in repair mechanisms, such as ATM/ATR, BER, and NER ...
Anu Singh, Aroonima Misra, Sufian Zaheer
wiley   +1 more source

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