The control of T-cell survival is of overwhelming importance for preventing leukemia and lymphoma. The present report demonstrates that the serine/threonine protein phosphatase PP4 regulates the survival of both leukemic T-cells and untransformed human peripheral blood T-cells, particularly after treatment with anti-leukemic drugs and other cytotoxic stimuli. PP4-induced apoptosis is mediated, at least in part, through de-phosphorylation of apoptosis regulator PEA-15, previously implicated in the control of leukemic cell survival. PP4 activity significantly affects the mutation rate in leukemic T-cells, indicating that PP4 dysfunction may be important in the development and progression of leukemia.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2734887 | PMC |
http://dx.doi.org/10.1016/j.leukres.2009.05.013 | DOI Listing |
Nucleic Acids Res
January 2025
Guangdong Provincial Key Laboratory of Digestive Cancer Research, Digestive Diseases Center, Scientific Research Center, The Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong 518107, P.R. China.
CRISPR-Cas12a technology has transformative potential, but as its applications grow, enhancing its inherent functionalities is essential to meet diverse demands. Here, we reveal a regulatory mechanism for LbCas12a through direct repeat (DR) region 3' end modifications and de-modifications, which can regulate LbCas12a's cis- and trans-cleavage activities. We extensively explored the effects of introducing phosphorylation, DNA, photo-cleavable linker, DNA modifications at the DR 3' end on LbCas12a's functionality.
View Article and Find Full Text PDFBiomed Mater
January 2025
School of Food Science and Technology, Dalian Polytechnic University, SKL of Marine Food Processing & Safety Control, National Engineering Research Center of Seafood, Dalian 116034, People's Republic of China.
Bone morphogenetic protein 2 (BMP-2) and a polysaccharide (SUP) were embedded in the calcium phosphate cement (CPC) scaffold, and the bone repair ability was evaluated. The new scaffolds were characterized using x-ray diffraction, Fourier transform-infrared, scanning electron microscopy, and energy dispersive spectroscopy analyses. CPC-BMP2-SUPH scaffold promoted the BMP-2 release by 1.
View Article and Find Full Text PDFOnco Targets Ther
January 2025
Department of Pharmacology, adMare BioInnovations, Montréal, Quebec, H4S 1Z9, Canada.
The gene is nearly ubiquitously subjected to activating mutation in pancreatic adenocarcinomas (PDAC), occurring at a frequency of over 90% in tumors. Mutant KRAS drives sustained signaling through the MAPK pathway to affect frequently disrupted cancer phenotypes including transcription, proliferation and cell survival. Recent research has shown that PDAC tumor growth and survival required a guanine nucleotide exchange factor for RAS homolog family member A (RhoA) called GEF-H1.
View Article and Find Full Text PDFSci Adv
January 2025
Key Laboratory of Plant Carbon Capture, Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences, Shanghai 200032, China.
Plants sense and respond to hyperosmotic stress via quick activation of sucrose nonfermenting 1-related protein kinase 2 (SnRK2). Under unstressed conditions, the protein phosphatase type 2C (PP2C) in clade A interact with and inhibit SnRK2s in subgroup III, which are released from the PP2C inhibition via pyrabactin resistance 1-like (PYL) abscisic acid receptors. However, how SnRK2s are released under osmotic stress is unclear.
View Article and Find Full Text PDFJ Cancer Res Clin Oncol
January 2025
Key Laboratory of Laboratory Medicine, Ministry of Education of China, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Purpose: Growing evidence suggests that the tyrosine phosphatase SHP2 is pivotal for tumor progression. Triple-negative breast cancer (TNBC) is the most lethal subtype of breast cancer, characterized by its high recurrence rate, aggressive metastasis, and resistance to chemotherapy. Understanding the mechanisms of tumorigenesis and the underlying molecular pathways in TNBC could aid in identifying new therapeutic targets.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!