Functional and structural insights into RAS effector proteins
RAS proteins are conserved guanosine triphosphate (GTP) hydrolases (GTPases) that act
as molecular binary switches and play vital roles in numerous cellular processes. Upon GTP …
as molecular binary switches and play vital roles in numerous cellular processes. Upon GTP …
Novel therapeutic perspectives in Noonan syndrome and RASopathies
C Saint-Laurent, L Mazeyrie, A Yart… - European Journal of …, 2024 - Springer
Noonan syndrome belongs to the family of RASopathies, a group of multiple congenital
anomaly disorders caused by pathogenic variants in genes encoding components or …
anomaly disorders caused by pathogenic variants in genes encoding components or …
Complex interplay between RAS GTPases and RASSF effectors regulates subcellular localization of YAP
S Singh, G Bernal Astrain, AM Hincapie… - EMBO …, 2024 - embopress.org
RAS GTPases bind effectors to convert upstream cues to changes in cellular function.
Effectors of classical H/K/NRAS are defined by RBD/RA domains which recognize the GTP …
Effectors of classical H/K/NRAS are defined by RBD/RA domains which recognize the GTP …
Small molecule inhibition for RASopathy-associated hypertrophic cardiomyopathy: Clinical application of a basic concept
D Chaput, G Andelfinger - Canadian Journal of Cardiology, 2024 - Elsevier
The term RASopathies designates a group of developmental syndrome that are caused by
activating variants of the RAS/MAPK cascade. The most prevalent clinical diagnosis is …
activating variants of the RAS/MAPK cascade. The most prevalent clinical diagnosis is …
RASopathies in Cardiac Disease
S Chennappan, MI Kontaridis - Annual Review of Medicine, 2024 - annualreviews.org
RASopathies are a group of clinically overlap** autosomal dominant disorders caused
primarily by mutations in genes that reside along the canonical Ras–mitogen-activated …
primarily by mutations in genes that reside along the canonical Ras–mitogen-activated …
Inhibition and degradation of NRAS with a pan-NRAS monobody
M Whaby, G Ketavarapu, A Koide, M Mazzei, M Mintoo… - Oncogene, 2024 - nature.com
The RAS family GTPases are the most frequently mutated oncogene family in human
cancers. Activating mutations in either of the three RAS isoforms (HRAS, KRAS, or NRAS) …
cancers. Activating mutations in either of the three RAS isoforms (HRAS, KRAS, or NRAS) …
RIT1 Promotes the Proliferation of Gliomas Through the Regulation of the PI3K/AKT/c‐Myc Signalling Pathway
Z Liu, H Jiang, H Kan, L Zhang, Y Rao… - Journal of Cellular …, 2025 - Wiley Online Library
Recently, RIT1 has been implicated in a range of neurological disorders; however, its
precise function in glioma pathogenesis is not yet well‐defined. This study employed …
precise function in glioma pathogenesis is not yet well‐defined. This study employed …
[HTML][HTML] Biochanin A inhibits cardiac hypertrophy and fibrosis in vivo and in vitro
Z Feng, N Zhang, J Bai, Q Lin, Y **e, Y **a - Biomedicine & …, 2024 - Elsevier
The heart undergoes pathological cardiac hypertrophy as an adaptive response to
prolonged pathological stimulation, leading to cardiomyocyte hypertrophy, fibroblast …
prolonged pathological stimulation, leading to cardiomyocyte hypertrophy, fibroblast …
[HTML][HTML] Dysregulation of RAS proteostasis by autosomal-dominant LZTR1 mutation induces Noonan syndrome–like phenotypes in mice
T Abe, K Morisaki, T Niihori, M Terao, S Takada… - JCI …, 2024 - pmc.ncbi.nlm.nih.gov
Leucine-zipper–like posttranslational regulator 1 (LZTR1) is a member of the BTB-Kelch
superfamily, which regulates the RAS proteostasis. Autosomal dominant (AD) mutations in …
superfamily, which regulates the RAS proteostasis. Autosomal dominant (AD) mutations in …
The deubiquitinase USP9X regulates RIT1 protein abundance and oncogenic phenotypes
RIT1 is a rare and understudied oncogene in lung cancer. Despite structural similarity to
other RAS GTPase proteins such as KRAS, oncogenic RIT1 activity does not appear to be …
other RAS GTPase proteins such as KRAS, oncogenic RIT1 activity does not appear to be …