Results 11 to 20 of about 2,366 (190)

MicroRNA-1185 Induces Endothelial Cell Apoptosis by Targeting UVRAG and KRIT1 [PDF]

open access: yesCellular Physiology and Biochemistry, 2017
Background/Aims: Atherosclerosis is a multifactorial chronic disease and is the main cause of death and impairment in the world. Endothelial injury and apoptosis play a crucial role in the onset and development of atherosclerosis. MicroRNAs (miRNAs) have
Haoyuan Deng   +9 more
doaj   +3 more sources

Correction: KRIT1 Regulates the Homeostasis of Intracellular Reactive Oxygen Species.

open access: yesPLoS ONE, 2019
[This corrects the article DOI: 10.1371/journal.pone.0011786.].
PLOS ONE staff
doaj   +3 more sources

GERM-LINE/SOMATIC DNA COMPARISON IN SPORADIC PATIENTS WITH CEREBRAL CAVERNOUS MALFORMATIONS.

open access: yesEuromediterranean Biomedical Journal, 2017
Cerebral cavernous malformations (CCMs) are benign tumours that affect brain capillaries. Although many cases remain asymptomatic, their incidence is steadily increasing.
Ivan Anchesi
doaj   +3 more sources

KRIT1 loss of function causes a ROS-dependent upregulation of c-Jun [PDF]

open access: yesFree Radical Biology and Medicine, 2014
Loss-of-function mutations in the KRIT1 gene (CCM1) have been associated with the pathogenesis of cerebral cavernous malformations (CCM), a major cerebrovascular disease.
Biasi, Fiorella   +9 more
core   +5 more sources

Familial Cerebral Cavernous Malformations: Pathophysiology, Genetics, Biomarkers, and Treatment Perspectives. [PDF]

open access: yesJ Neurochem
Cerebral cavernous malformations (CCMs) are vascular lesions in the brain caused by inherited genetic mutations in the CCM1/2/3 genes that disrupt normal blood vessel function. This work demonstrates that these mutations lead to endothelial dysfunction, inflammation, and iron accumulation, which can be detected by magnetic resonance imaging (MRI) and ...
Fontes-Dantas FL   +5 more
europepmc   +2 more sources

KRIT1 in vascular biology and beyond. [PDF]

open access: yesBiosci Rep
Abstract KRIT1 is a 75 kDa scaffolding protein which regulates endothelial cell phenotype by limiting the response to inflammatory stimuli and maintaining a quiescent and stable endothelial barrier. Loss-of-function mutations in KRIT1 lead to the development of cerebral cavernous malformations (CCM), a disease marked by the formation ...
Glading AJ.
europepmc   +3 more sources

Cerebral Cavernous Malformation: From Genetics to Pharmacotherapy. [PDF]

open access: yesBrain Behav
CCM1, CCM2, CCM3, MAP3K3, and PIK3CA genes mediate CCM pathogenesis by regulating the RhoA–ROCK, MAP3K3–KLF2/4, and PIK3CA–AKT–mTOR pathways, affecting processes such as cell migration, intercellular junctions, cell proliferation, inflammation, autophagy, EndMT, angiogenesis, and oxidative stress.
Zhang Z, Deng J, Sun W, Wang Z.
europepmc   +2 more sources

Protein kinase Cα regulates the nucleocytoplasmic shuttling of KRIT1 [PDF]

open access: yesFree Radical Biology and Medicine, 2021
ABSTRACT KRIT1 is a scaffolding protein that regulates multiple molecular mechanisms, including cell–cell and cell–matrix adhesion, and redox homeostasis and signaling. However, rather little is known about how KRIT1 is itself regulated.
Elisa De Luca   +9 more
openaire   +3 more sources

KRIT1 Deficiency Promotes Aortic Endothelial Dysfunction [PDF]

open access: yesInternational Journal of Molecular Sciences, 2019
Loss-of-function mutations of the gene encoding Krev interaction trapped protein 1 (KRIT1) are associated with the pathogenesis of Cerebral Cavernous Malformation (CCM), a major cerebrovascular disease characterized by abnormally enlarged and leaky capillaries and affecting 0.5% of the human population. However, growing evidence demonstrates that KRIT1
Vieceli Dalla Sega F.   +14 more
openaire   +2 more sources

Next-Generation Sequencing Advances the Genetic Diagnosis of Cerebral Cavernous Malformation (CCM)

open access: yesAntioxidants, 2022
Cerebral Cavernous Malformation (CCM) is a cerebrovascular disease of genetic origin that predisposes to seizures, focal neurological deficits and fatal intracerebral hemorrhage. It may occur sporadically or in familial forms, segregating as an autosomal
Valerio Benedetti   +6 more
doaj   +1 more source

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