Results 61 to 70 of about 40,983 (302)

PICALM::MLLT10 translocated leukemia

open access: yesFEBS Letters, EarlyView.
This comprehensive review of PICALM::MLLT10 translocated acute leukemia provides an in‐depth review of the structure and function of CALM, AF10, and the fusion oncoprotein (1). The multifaceted molecular mechanisms of oncogenesis, including nucleocytoplasmic shuttling (2), epigenetic modifications (3), and disruption of endocytosis (4), are then ...
John M. Cullen   +7 more
wiley   +1 more source

Cell density–dependent nuclear‐cytoplasmic shuttling of SETDB1 integrates with Hippo signaling to regulate YAP1‐mediated transcription

open access: yesFEBS Letters, EarlyView.
At low cell density, SETDB1 and YAP1 accumulate in the nucleus. As cell density increases, the Hippo pathway is gradually activated, and SETDB1 is associated with increased YAP1 phosphorylation. At high cell density, phosphorylated YAP1 is sequestered in the cytoplasm, while SETDB1 becomes polyubiquitinated and degraded by the ubiquitin–proteasome ...
Jaemin Eom   +3 more
wiley   +1 more source

Theoretical Principles of Multiscale Spatiotemporal Control of Neuronal Networks: A Complex Systems Perspective

open access: yesFrontiers in Computational Neuroscience, 2018
Success in the fine control of the nervous system depends on a deeper understanding of how neural circuits control behavior. There is, however, a wide gap between the components of neural circuits and behavior.
Nima Dehghani, Nima Dehghani
doaj   +1 more source

β‐TrCP overexpression enhances cisplatin sensitivity by depleting BRCA1

open access: yesMolecular Oncology, EarlyView.
Low levels of β‐TrCP (Panel A) allow the accumulation of BRCA1 and CtIP, which facilitate the repair of cisplatin‐induced DNA damage via homologous recombination (HR) and promote tumor cell survival. In contrast, high β‐TrCP expression (Panel B) leads to BRCA1 and CtIP degradation, impairing HR repair, resulting in persistent DNA damage and apoptosis ...
Rocío Jiménez‐Guerrero   +8 more
wiley   +1 more source

Emerging role of ARHGAP29 in melanoma cell phenotype switching

open access: yesMolecular Oncology, EarlyView.
This study gives first insights into the role of ARHGAP29 in malignant melanoma. ARHGAP29 was revealed to be connected to tumor cell plasticity, promoting a mesenchymal‐like, invasive phenotype and driving tumor progression. Further, it modulates cell spreading by influencing RhoA/ROCK signaling and affects SMAD2 activity. Rho GTPase‐activating protein
Beatrice Charlotte Tröster   +3 more
wiley   +1 more source

Temporal Asymmetry, Entropic Irreversibility, and Finite-Time Thermodynamics: From Parmenides–Einstein Time-Reversal Symmetry to the Heraclitan Entropic Arrow of Time

open access: yesEntropy, 2012
In this paper, we combine the two universalisms of thermodynamics and dynamical systems theory to develop a dynamical system formalism for classical thermodynamics. Specifically, using a compartmental dynamical system energy flow model we develop a state-
Wassim M. Haddad
doaj   +1 more source

Modern Dynamical Systems Theory [PDF]

open access: yesSymposium - International Astronomical Union, 1974
In order to analyse generic or typical properties of dynamical systems we consider the space of all C1-vector fields on a fixed differentiable manifold M. In the C1-metric, assuming M is compact, is a complete metric space and a generic subset is an open dense subset or an intersection of a countable collection of such open dense subsets of .
openaire   +1 more source

CDK11 inhibition induces cytoplasmic p21WAF1 splice variant by p53 stabilisation and SF3B1 inactivation

open access: yesMolecular Oncology, EarlyView.
CDK11 inhibition stabilises the tumour suppressor p53 and triggers the production of an alternative p21WAF1 splice variant p21L, through the inactivation of the spliceosomal protein SF3B1. Unlike the canonical p21WAF1 protein, p21L is localised in the cytoplasm and has reduced cell cycle‐blocking activity.
Radovan Krejcir   +12 more
wiley   +1 more source

Class IIa HDACs forced degradation allows resensitization of oxaliplatin‐resistant FBXW7‐mutated colorectal cancer

open access: yesMolecular Oncology, EarlyView.
HDAC4 is degraded by the E3 ligase FBXW7. In colorectal cancer, FBXW7 mutations prevent HDAC4 degradation, leading to oxaliplatin resistance. Forced degradation of HDAC4 using a PROTAC compound restores drug sensitivity by resetting the super‐enhancer landscape, reprogramming the epigenetic state of FBXW7‐mutated cells to resemble oxaliplatin ...
Vanessa Tolotto   +13 more
wiley   +1 more source

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