Investigating transcription factor dynamics in health and disease using FRAP
FEBS Letters, EarlyView.FRAP analysis of GFP‐tagged transcription factors reveals how molecular mobility and target engagement change in response to drug treatment. By combining live‐cell imaging, quantitative model fitting, and statistical analysis, this approach uncovers transcription factor dynamics linked to disease mechanisms, providing a powerful framework for ...
Kannan Govindaraj +3 more
wiley +1 more source
Phosphorylation by Akt within the ST loop of AMPK-α1 down-regulates its activation in tumour cells [PDF]
, 2014 The insulin/IGF-1 (insulin-like growth factor 1)-activated protein kinase Akt (also known as protein kinase B) phosphorylates Ser487 in the ‘ST loop’ (serine/threonine-rich loop) within the C-terminal domain of AMPK-a1 (AMP-activated protein kinase-a1 ...
Leslie, Nicholas R. +6 more
core +1 more source
An epithelial GPR35 isoform supports tumor‐associated transcriptional and metabolic phenotypes
FEBS Letters, EarlyView.GPR35 generates two functionally distinct isoforms with previously unresolved roles. GPR35‐short mediates immune‐cell chemotaxis, while GPR35‐long is enriched in colorectal cancer epithelium, where it supports increased metabolism, proliferation, and tumor‐associated transcriptional programs.
Jørgen D. Rønneberg +14 more
wiley +1 more source
Genome-wide analysis to predict protein sequence variations that change phosphorylation sites or their corresponding kinases [PDF]
, 2008 We define phosphovariants as genetic variations that change phosphorylation sites or their interacting kinases. Considering the essential role of phosphorylation in protein functions, it is highly likely that phosphovariants change protein functions and ...
Pamela Song +4 more
core
PIM1-dependent phosphorylation of Histone H3 at Serine 10 is required for MYC-dependent transcriptional activation and oncogenic transformation. [PDF]
, 2007 The serine/threonine kinase PIM1, cooperates with MYC in cell cycle progression and tumorigenesis. However, the nature of this cooperation remains elusive.
Salvatore Oliviero +7 more
core +1 more source
Discerning protein pools by selective staining with self‐labeling tags
FEBS Letters, EarlyView.Cell surface proteins have an intra‐ and extracellular pool. Combining genetic fusion to self‐labeling tags that can be addressed with small molecule fluorophores allows separating these pools. We highlight recent developments and techniques for state‐of‐the‐art interrogation of cell surface proteins in the complex tissue setting.
Kati Fischermanns, Johannes Broichhagen
wiley +1 more source
βTrCP-mediated proteolysis of NF-kB1 p105 requires phosphorylation of p105 serines 927 and 932 [PDF]
, 2003 This work was supported by the U.K. Medical Research Council, the Arthritis Research Campaign (project grant L0536 to V.L.), and the AINP consortium, EC—5th framework.NF-κB1 p105 functions both as a precursor of NF-κB1 p50 and as a cytoplasmic inhibitor ...
Ben-Neriah, Yinon +9 more
core +1 more source
FEBS Letters, EarlyView.Animals must match their growth rate to available nutrients. We show that in Drosophila larvae, the nutrient‐sensing TOR kinase controls growth by regulating levels of TFAM, a key regulator of mitochondrial function, in the adipose tissue. When nutrients are abundant, high TOR activity suppresses TFAM, lowering mitochondrial bioenergetic activity and ...
Shrivani Sriskanthadevan‐Pirahas +4 more
wiley +1 more source
Crosstalk of protein phosphorylation and lysine acetylation on 14-3-3 proteins and their applications in brassinosteroid signaling and photosynthesis [PDF]
, 2011 Protein phosphorylation and lysine acetylation are two important post-translational modifications (PTMs) in eukaryotes. However, the crosstalk between these two modifications is largely unknown.
Wu, Xia
core
Epigenetic reprogramming of lineage switching in cancer
FEBS Letters, EarlyView.Cancer cells rarely commit to a single identity. Epigenetic mechanisms and tumor microenvironment cues push epithelial cells toward flexible, hybrid states that can shift into mesenchymal, neuroendocrine, or stem‐like fates, driving metastasis, drug resistance, and tumor heterogeneity. Targeting the epigenetic regulators behind these transitions, using
Ezgi Boyvatlı +4 more
wiley +1 more source