Results 171 to 180 of about 81,917 (261)

Fulminant Myocarditis Presenting With Refractory Ventricular Fibrillation During BRAF/MEK Inhibitor Therapy. [PDF]

JACC Case Rep
Lalario A, Rubbo FM, Bassetto G, Mazzaro E, Pinamonti M, Bussani R, Sinagra G, Stolfo D.   +7 more
europepmc   +1 more source

BRAF inhibitor or BRAF/MEK inhibitor treatment for patients with metastatic BRAF V600E mutated differentiated thyroid cancer. [PDF]

Arch Endocrinol Metab
Finkel I, Korzets Y, Moore A, Coreanu T, Popovtzer A, Shoffel-Havakuk H, Bachar G, Mansour J, Weiss C, Robenshtok E.   +9 more
europepmc   +1 more source

Inhibition of MCL-1 and MEK Overcomes MEK Inhibitor Resistance in Triple-Negative and Inflammatory Breast Cancers. [PDF]

Mol Cancer Ther
Mughees M, Tacam M, Tan AW, Pitner MK, Iles LR, Hu X, Villodre ES, Debeb BG, Kogawa T, Lim B, Layman RM, Woodward WA, Ueno NT, Tripathy D, Krishnamurthy S, Qi Y, Pusztai L, Wang J, Gandhi V, Bartholomeusz G, Bartholomeusz C.   +20 more
europepmc   +1 more source

GSK3α‐mediated regulation of the RNA demethylase fat mass and obesity‐associated protein (FTO) during murine spermatogenesis

The FEBS Journal, EarlyView.
FTO regulates mRNA stability and translational efficiency through its m6A‐demethylation activity. GSK3 functions as an upstream regulator of FTO, leading to its inhibition via phosphorylation. In male germ cells, FTO activity is kept in check by GSK3α.
Neha Choudhari, Budheswar Dehury, Rounak Roy, Radhakrishnan Periyasamy, Indrashis Bhattacharya, Mahesh Sahare, Srinivasan Vijayraghavan, Souvik Dey   +7 more
wiley   +1 more source

Risk of developing malignant peripheral nerve sheath tumors in patients with neurofibromatosis 1 receiving MEK inhibitor treatment for plexiform neurofibromas. [PDF]

Neurooncol Adv
Sankaran H, Dombi E, Glassberg B, Baldwin A, Heisey K, Dufek A, Tibery C, Best AF, Chen AP, Widemann BC, Gross AM.   +10 more
europepmc   +1 more source

A guide to transcriptional cyclin‐dependent kinases in cancer

The FEBS Journal, EarlyView.
Transcriptional cyclin‐dependent‐kinases (tCDKs) facilitate gene expression by promoting RNA polymerase II (RNAPII) progression through discrete phases of the transcription cycle. Aberrant tCDK activity is detectable in different human cancers, thereby contributing to de‐regulated gene expression programs that drive oncogenic phenotypes.
Jennifer R. Devlin, Salla Kyheröinen, Ricky W. Johnstone   +2 more
wiley   +1 more source

Molecular Evidence Supporting MEK Inhibitor Therapy in NF1 Pseudarthrosis. [PDF]

J Bone Joint Surg Am
Paria N, Oxendine I, Podeszwa D, Wassell M, Cornelia R, Wise CA, Rios JJ.   +6 more
europepmc   +1 more source

A comparative analysis of cell death signalling in RNA and DNA virus infections and potential inhibitory strategies

The FEBS Journal, EarlyView.
RNA and DNA viruses can manipulate host cell death through various mechanisms. RNA viruses (H1N1, SARS‐CoV‐2) induce acute apoptosis, necroptosis, and pyroptosis to promote rapid viral transmission and epithelial barrier damage. In contrast, DNA viruses (HSV‐1, EBV) regulate these mechanisms to sustain a lytic‐latency cycle, evade immune response and ...
Panagiotis Keramidas, Maria Pitou, Amalia Aggeli, Sotiris Varlamis, Theodora Choli‐Papadopoulou   +4 more
wiley   +1 more source

Anti-tumor efficacy of RAF/MEK inhibitor VS6766 in KRAS-mutated colorectal cancer cells. [PDF]

Cancer Chemother Pharmacol
Zhu H, Yan G, Ma J, Zhang B, Yan Y, Zhu L, Dong R, Lin N, Tan B.   +8 more
europepmc   +1 more source

Kinetic signatures of RAS–BRAF engagement reveal isoform selectivity, oncogenic amplification, and mutation‐dependent inhibitor resistance

The FEBS Journal, EarlyView.
The BRAF N terminus uses a cooperative BSR–CRD gate that restricts RAS binding to the RBD, which can be mitigated by oncogenic RAS mutations. KRAS engages BRAF through stability‐driven, long‐lived complexes, whereas NRAS binds transiently in a frequency‐driven mode.
Sravani Malasani, Zhihong Wang
wiley   +1 more source