Results 51 to 60 of about 4,575,740 (255)

On ARS-interacting multifunctional protein p18 [PDF]

open access: yes, 2008
Nine aminoacyl-tRNA synthetases with three auxiliary components are forming a multisynthetase complex which is essential component of protein biosynthesis machinery. The smallest auxiliary component p18 takes part in biosynthesis channeling. It is also a
Viktor Deineko
core   +1 more source

MITF maintains genome stability in nonmelanocyte lineages

open access: yesMolecular Oncology, EarlyView.
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir   +13 more
wiley   +1 more source

Immunohistochemistry Assessment of P53 Protein in Basal Cell Carcinoma

open access: yesIranian Journal of Allergy, Asthma and Immunology, 2005
The most frequently mutated tumor suppressor gene found in human cancer is p53. In a normal situation, p53 is activated upon the induction of DNA damage to either arrest the cell cycle or else induce apoptosis.
Reza Ghaderi Fatemeh Haghighi
doaj  

Cell-to-cell transmission of p53 aggregates: a novel player in oncology?

open access: yesMolecular & Cellular Oncology, 2021
The mutants of the tumor suppressor protein p53 form protein aggregates. It has been proposed that these aggregates propagate like prions, albeit the detailed mechanism of the propagation is unclear.
Naoyuki Iwahashi   +4 more
doaj   +1 more source

A Second Career for p53 as A Broad-Spectrum Antiviral?

open access: yesViruses, 2023
As the world exits the global pandemic caused by the previously unknown SARS-CoV-2, we also mark the 30th anniversary of p53 being named “molecule of the year” by Science based on its role as a tumor suppressor.
Joe B. Harford
doaj   +1 more source

Gain-of-function oncogenic mutations in TP53 enhance defined factor-mediated cellular reprogramming [PDF]

open access: yes, 2011
Cancer is a disorder with various genetic and epigenetic alterations. Genetic alterations such as mutations, i.e., substitutions, amplifications, and deletions of nucleotide sequences, are largely irreversible, whereas epigenetic alterations can be ...
Kazuyoshi Yamamoto   +8 more
core   +1 more source

A novel quinazolinone insulin receptor inhibitor and its synergy with an EGFR inhibitor in glucose‐driven glioblastoma

open access: yesMolecular Oncology, EarlyView.
The novel styrylquinazolinone‐based molecule W1B effectively suppresses glioblastoma by inhibiting IGF1R and EGFR. In high‐glucose microenvironments driving tumor resistance, W1B acts synergistically with the EGFR inhibitor dacomitinib. This combination safely blocks compensatory survival signaling in zebrafish xenograft models. Showcasing promising in
Patryk Rurka   +9 more
wiley   +1 more source

Crucial role of TSC-22 in preventing the proteasomal degradation of p53 in cervical cancer. [PDF]

open access: yesPLoS ONE, 2012
The p53 tumor suppressor function can be compromised in many tumors by the cellular antagonist HDM2 and human papillomavirus oncogene E6 that induce p53 degradation. Restoration of p53 activity has strong therapeutic potential. Here, we identified TSC-22
Cheol-Hee Yoon   +9 more
doaj   +1 more source

Comparison of p53 Protein Expression between Oral Squamous Cell Carcinoma and Verrucous Carcinoma

open access: yesRUHS Journal of Health Sciences, 2023
Introduction: Deletion or mutation of tumor suppressor genes plays a significant role in cancer development. Mutation of the p53 tumor suppressor gene is the most common genetic alteration associated with oral cancer. The aim of this study was to compare
Anil Singh; Shikha Saxena; Safia Siddiqui; Ruchita Bali; Priyanka Singh
doaj   +1 more source

Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization

open access: yesMolecular Oncology, EarlyView.
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu   +13 more
wiley   +1 more source

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