Results 41 to 50 of about 602,797 (262)

CEACAM1 participation in breast cancer progression

open access: yesMolecular Oncology, EarlyView.
In invasive breast cancer (BC), CEACAM1 shifts from an apical to a uniform membranous/cytoplasmic pattern, or is lost, as tumors dedifferentiate, inversely tracking the Ki‐67 proliferative index. In MCF‐7 cells, only CEACAM1‐4L suppresses proliferation, repressing cell cycle and growth factor genes.
Mykola Lyndin   +3 more
wiley   +1 more source

PANoptosis in the pathogenesis of myelodysplastic syndromes

open access: yesMolecular Oncology, EarlyView.
PANoptosis, a combination of three types of programmed cell death, is mediated by a large protein complex called a PANoptosome. In healthy bone marrow hematopoietic cells, PANoptosis is restricted by inhibitory signaling. In MDS, bone marrow cells become sensitive to the PANoptotic stimuli due to the aberrant inactivation of inhibitory signaling or ...
Rohit Thalla   +4 more
wiley   +1 more source

Cloning and Sequencing cDNA Encoding for Rhoptry-2 Toxoplasma Gondii Tachyzoite Local Isolate

open access: yesIndonesian Journal of Biotechnology, 2008
Rhoptry protein belongs to an excretory and secretory antigens (ESAs) that play an important role during active penetration of parasite into the cell target.
M. Murwantoko   +2 more
doaj   +1 more source

Partial FAK suppression promotes tumor growth, an effect reversed by macrophage p110δ PI3K inactivation

open access: yesMolecular Oncology, EarlyView.
Partial inhibition of focal adhesion kinase (FAK) can paradoxically promote tumor growth, rather than simply producing a weaker antitumor effect than that observed with strong FAK suppression. In breast cancer and melanoma models, targeting p110δ PI3K, particularly in macrophages, counteracted these tumor‐promoting effects, highlighting the importance ...
Lydia Xenou   +4 more
wiley   +1 more source

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

open access: yesMolecular 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   +7 more
wiley   +1 more source

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

open access: yesMolecular 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   +2 more
wiley   +1 more source

Genomic presence of recombinant porcine endogenous retrovirus in transmitting miniature swine

open access: yesVirology Journal, 2006
The replication of porcine endogenous retrovirus (PERV) in human cell lines suggests a potential infectious risk in xenotransplantation. PERV isolated from human cells following cocultivation with porcine peripheral blood mononuclear cells is a ...
Wilkinson Robert   +2 more
doaj   +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

open access: yesMolecular 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   +17 more
wiley   +1 more source

Cloning, Expression and Toxicity of a Mosquitocidal Toxin Gene of Bacillus thuringiensis subsp. medellin

open access: yesMemorias do Instituto Oswaldo Cruz, 1997
Bacillus thuringiensis (Bt) subsp. medellin (Btmed) produces parasporal crystalline inclusions which are toxic to mosquito larvae. It has been shown that the inclusions of this bacterium contain mainly proteins of 94, 68 and 28-30 kDa.
Nora Restrepo   +5 more
doaj   +1 more source

Mutant p53R273H disrupts PDPK1 homodimerization and contributes to PDPK1 activation

open access: yesMolecular 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   +11 more
wiley   +1 more source

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