Results 51 to 60 of about 204,002 (257)
Generation of pulsatile ERK activity in mouse embryonic stem cells is regulated by Raf activity
The extracellular signal-regulated kinase (ERK) is a serine/threonine kinase that is known to regulate cellular events such as cell proliferation and differentiation.
Yayoi Toyooka +5 more
doaj +1 more source
Epigenetic reprogramming of lineage switching in cancer
Cancer cells rarely commit to a single identity. Epigenetic mechanisms and tumor microenvironment cues push epithelial cells toward flexible, hybrid states that can shift into mesenchymal, neuroendocrine, or stem‐like fates, driving metastasis, drug resistance, and tumor heterogeneity. Targeting the epigenetic regulators behind these transitions, using
Ezgi Boyvatlı +4 more
wiley +1 more source
Aedes mosquitoes can transmit dengue and several other severe vector-borne viral diseases, thereby influencing millions of people worldwide. Insects primarily control and clear the viral infections via their innate immune systems.
Wen-Quan Liu +12 more
doaj +1 more source
Ligand‐dependent transcriptional heterogeneity in cell cycle gene expression delays G1/S entry
EGF and HRG induce distinct G1/S progression programs in ErbB2‐amplified BT474 breast cancer cells. Despite activating the potent ErbB2–ErbB3 heterodimer, HRG does not accelerate cell‐cycle entry. Instead, EGF promotes earlier restriction‐point passage via ERK–FOS signaling, whereas HRG activates the AKT–MYC axis, driving transcriptional heterogeneity ...
Ririn Rahmala Febri +5 more
wiley +1 more source
Computational modelling of cancerous mutations in the EGFR/ERK signalling pathway [PDF]
The Epidermal Growth Factor Receptor (EGFR) activated Extracellular-signal Regulated Kinase (ERK) pathway is a critical cell signalling pathway that relays the signal for a cell to proliferate from the plasma membrane to the nucleus. Deregulation of the EGFR/ERK pathway due to alterations affecting the expression or function of a number of pathway ...
Richard J. Orton +5 more
openaire +5 more sources
The role of miR‐335‐5p in the redifferentiation of BRAF p.V600E thyroid cancers
The BRAF p.V600E mutation promotes thyroid cancer dedifferentiation and radioiodine resistance. Using a network approach, we identified miR‐335‐5p as a key regulator of BRAF‐mutated thyroid tumors. Restoring miR‐335‐5p increased thyroid‐specific gene expression and iodine uptake in cells and organoids.
Valeria Pecce +11 more
wiley +1 more source
Tug-of-war via ERK signaling pathway for tissue organization – ERK activation to force generation
Extracellular signal-regulated kinase (ERK) plays a crucial role in regulating collective cell behaviors observed in diverse biological phenomena. Emerging studies have shed light on the involvement of the ERK signaling pathway in the reception and generation of mechanical forces, thereby governing local mechanical interactions within multicellular ...
Ankita Nitin Nayak, Tsuyoshi Hirashima
openaire +2 more sources
Dormant cancer cells can hide in distant organs for years, evading treatment and the immune system. This review highlights how signals from the surrounding tissue and immune environment keep these cells inactive or trigger their reawakening. Understanding these mechanisms may help develop therapies to eliminate or control dormant cells and prevent ...
Kanishka Tiwary +1 more
wiley +1 more source
Systemic Perturbation of the ERK Signaling Pathway by the Proteasome Inhibitor, MG132
Inhibition of the ubiquitin-proteasome protein degradation pathway has been identified as a viable strategy for anti-tumor therapy based on its broad effects on cell proliferation. By the same token, the variety of elicited effects confounds the interpretation of cell-based experiments using proteasome inhibitors such as MG132.
Murat Cirit, Kyle G Grant, Jason M Haugh
openaire +4 more sources
Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis +3 more
wiley +1 more source

