Results 151 to 160 of about 11,155,248 (357)

Ras-mediated phosphorylation of a conserved threonine residue enhances the transactivation activities of c-Ets1 and c-Ets2 [PDF]

, 1996
The Ras oncogene products regulate the expression of genes in transformed cells, and members of the Ets family of transcription factors have been implicated in this process.
Yang, Beom-Seok, Ostrowski, M C, Hauser, C A, Hauser, Craig A., Van Beveren, Charles, Maki, R A, Yang, B S, Henkel, G, Hume, D A, Ostrowski, Michael C., Colman, M S, Colman, Michael S., Van Beveren, C, Henkel, Gregory, Stacey, K J, Hume, David A., Maki, Richard A., Stacey, Katryn J.   +17 more
core   +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

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

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

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

Paclitaxel induces NM2‐dependent cellular contraction through GEF‐H1 dissociation from microtubules and RhoA/ROCK activation in cancer cells

Molecular Oncology, EarlyView.
Taxanes are widely used chemotherapeutics whose effects on cellular mechanics remain poorly understood. We show that paclitaxel induces rapid cellular contraction by promoting GEF‐H1 dissociation from microtubules and non‐muscle myosin II activation through RhoA/ROCK.
Gloria Asensio‐Juárez, Rafael Pérez‐Díaz, Hugo Ramos‐Solano, Marina Garrido‐Casado, Vanessa C. Talayero, Miguel Vicente‐Manzanares   +5 more
wiley   +1 more source

SPHINX31 acts as a SRPK1 inhibitor targeting the ATR/DNA‐PKcs/CHK1 replicative checkpoint to inhibit cell growth in non‐small cell lung cancer

Molecular Oncology, EarlyView.
The kinase SRPK1 directly interacts with the protein TOPBP1 and regulates the pre‐mRNA splicing of WIZ thereby contributing to the activation of the ATR/CHK1 replicative checkpoint in response to replicative stress. This allows cancer cells' genomic stability and survival.
Amani Shreim, Aurelie Genoux, Nadiia Zubchuk, Haoyang Zheng, Perla Salameh, Theo Ziegelmeyer, Fabien Dalonneau, Margot Rouchette, Christiane Oddou, Simona Miron, Helene Polveche, Adiilah Mamode Cassim, Carmen Garrido, Eleni Nikolakaki, Didier Auboeuf, Tao Jia, Sophie Zinn‐Justin, Beatrice Eymin   +17 more
wiley   +1 more source

Mutant p53R273H disrupts PDPK1 homodimerization and contributes to PDPK1 activation

Molecular Oncology, EarlyView.
How mutant p53R273H drives AKT signaling is unclear. We show that p53R273H, but not wild‐type, directly binds PDPK1 via a mutation‐dependent conformational change. This interaction disrupts inhibitory PDPK1 homodimerization and enhances AKT phosphorylation.
Mei Chee Lim, Alvin Kunyao Guo, Yoko Itahana, Srinivasaraghavan Kannan, Valerie Goh, Mingmin Ong, Terina Yan Wen Tay, Weiying Ye, Sabhashina Radha Krishnan, Jun Nishiyama, Chandra S Verma, Koji Itahana   +11 more
wiley   +1 more source

Activation of AMPK as a therapeutic strategy for FBXL4-related mitochondrial DNA depletion syndrome

EMBO Molecular Medicine
Distinct mitophagy pathways can eliminate not only damaged mitochondria but also healthy ones. In Mitochondrial DNA Depletion Syndrome 13 (MTDPS13), dysregulated BNIP3/NIX-driven mitophagy of functional mitochondria is thought to be the key pathological ...
Aniketh Bishnu, Juan Zapata-Muñoz, Robert W Taylor, Kei Sakamoto, Ian G Ganley   +4 more
doaj   +1 more source

A large-scale protein phosphorylation analysis reveals novel phosphorylation motifs and phosphoregulatory networks in Arabidopsis

, 2013
Large-scale protein phosphorylation analysis by MS is emerging as a powerful tool in plant signal transduction research. However, our current understanding of the phosphorylation regulatory network in plants is still very limited.
JunXianHe, Bian, Yangyang, Gu, Li-Fei, Wang, Xu, Sun, Samuel Sai-Ming, Zou, Hanfa, 邹汉法, Ye, Mingliang, SamuelSaiMingSun, Cheng, Kai, He, Jun-Xian   +10 more
core   +1 more source