Results 201 to 210 of about 16,476,009 (293)

Develop a novel non-coplanar trajectory optimization algorithm for an efficient 4pi spot-scanning proton Arc (SPArc_-4pi) treatment delivery. [PDF]

Med Phys
Cong X, Chen S, Liu P, Chen P, Xu X, Li X, Chen P, Chinnaiyan P, Ding X.   +8 more
europepmc   +1 more source

Arginine methylation as a regulatory ratchet in cancer: From substrate selection to malignant‐state stabilization

Molecular Oncology, EarlyView.
Arginine methylation can be viewed as a persistence‐prone post‐translational modification regulated by a network of PRMTs. Competitive and compensatory interactions among PRMTs can redistribute methylation across substrate pools shaped by sequence, structural, spatial, and environmental layers, reinforcing RNA‐processing, chromatin, and signaling ...
So Hyun Kwon, Ji Min Lee
wiley   +1 more source

Reasonable Adjustments Across the Learning Disability Annual Health Check Pathway: A Co-designed Qualitative Study

Ditzel N, Howells K, Gorman L, Blakeman T, Gillibrand S, Sanders C, Chauhan U.   +6 more
europepmc   +1 more source

Quantitative Sodium MRI of the Human Patellar Tendon. [PDF]

NMR Biomed
Möller R, Jurisic J, Drewes LR, Ljimani A, Wittsack HJ, Nagel AM, Antoch G, Wilms LM, Müller-Lutz A, Kamp B.   +9 more
europepmc   +1 more source

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

Molecular Oncology, EarlyView.
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim, Maryam Aslam, Elouise Torruella, Alphons Sony, Asif Rahman, Simira Smith, Columba de la Parra, Moira Sauane   +7 more
wiley   +1 more source

The VHL tumor suppressor at the crossroad of protein folding, aggregation, and cancer

Molecular Oncology, EarlyView.
Mutations, environmental stress, and chaperone dysfunction can destabilize pVHL, promoting its conversion from the native folded state into amyloid‐like assemblies. This transition may contribute to protein storage, cell dormancy, survival, and drug resistance.
Lara Abad, Silvio Carlo Ermanno Tosatto, Emanuela Leonardi   +2 more
wiley   +1 more source

Direct oral anticoagulants after surgical bioprosthetic valve replacement or mitral repair: reconciling valve and atrial fibrillation guidelines. [PDF]

J Thorac Dis
Chevli PA, Bhave PD.
europepmc   +1 more source

NAPRT loss promotes lung tumor initiation and growth through AKT signaling independently of NAD+ biosynthesis

Molecular Oncology, EarlyView.
Loss of NAPRT promotes lung tumor initiation and growth through a noncanonical mechanism, independent of its role in NAD+ biosynthesis. Mechanistically, NAPRT depletion activates the mTORC2‐driven AKT/β‐catenin signaling axis to enhance clonogenic and invasive phenotypes. Furthermore, lung‐specific Naprt deletion significantly increases tumor burden in
Myung Joon Oh, Ji Yun Jang, Yoon Jeon, Gi‐Cheon Kim, Hwanho Lee, Jooyoung Lee, Ju‐Hwa Kim, Hakhyun Kim, Minjee Kim, Ho‐Keun Kwon, Ho Lee, Hyun Seok Kim   +11 more
wiley   +1 more source

Statutory construction and interpretation for AI. [PDF]

Proc Natl Acad Sci U S A
He L, Nadeem N, Liao M, Chen H, Chen D, Cuéllar MF, Henderson P.   +6 more
europepmc   +1 more source

Regulation of the lncRNA NEAT1 by p53‐ΔNp63 crosstalk modulates the DNA damage response and therapeutic efficacy in HNSCC

Molecular Oncology, EarlyView.
In head and neck squamous cell carcinoma (HNSCC) p53 and p63 exert opposite roles on the transcription regulation of the lncRNA NEAT1. Under basal conditions, p53 levels are low and p63 represses NEAT1 expression. Upon genotoxic stress, p53 is rapidly induced, displacing p63 from the NEAT1 promoter leading to NEAT1 transcriptional activation and ...
Sara De Domenico, Veronica La Banca, Silvia D'Amico, Stefano Scalera, Sara Nicolai, Angelo Peschiaroli   +5 more
wiley   +1 more source