Results 91 to 100 of about 63,382 (353)

CD47 promotes mitogen‐activated protein kinase and epithelial‐to‐mesenchymal transition molecular programs to drive prometastatic phenotypes in non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
Beyond its role in immune evasion, this study identified that CD47 drives tumor‐intrinsic signaling in non‐small cell lung cancer (NSCLC). Transcriptomic profiling and functional studies revealed that CD47 regulates cell adhesion, migration, and metastasis through an ERK–EMT signaling axis.
Asa P.Y. Lau   +8 more
wiley   +1 more source

hnRNPH2 as an Inhibitor of Chicken MDA5-Mediated Type I Interferon Response: Analysis Using Chicken MDA5–Host Interactome

open access: yesFrontiers in Immunology, 2020
RIG-I and MDA5 are two key pattern recognition receptors that sense the invasion of RNA viruses and initiate type I interferon (IFN) response. Although these receptors are generally conserved in vertebrates, RIG-I is absent in chickens, whereas MDA5 is ...
Xian Lin   +12 more
doaj   +1 more source

The IA-2 interactome [PDF]

open access: yesDiabetologia, 2005
Islet antigen-2 (IA-2), a major autoantigen in type 1 diabetes, is an enzymatically inactive member of the transmembrane protein tyrosine phosphatase (PTP) family. IA-2 is located in dense-core secretory vesicles and is involved in the regulation of insulin secretion.
Notkins, A. L.   +4 more
openaire   +3 more sources

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis   +3 more
wiley   +1 more source

Identification of disease treatment mechanisms through the multiscale interactome

open access: yesNature Communications, 2020
Most diseases disrupt multiple proteins, and drugs treat such diseases by restoring the functions of the disrupted proteins. How drugs restore these functions, however, is often unknown as a drug’s therapeutic effects are not limited to the proteins that
Camilo Ruiz, M. Zitnik, J. Leskovec
semanticscholar   +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

Defining the Helicobacter pylori Disease-Specific Antigenic Repertoire

open access: yesFrontiers in Microbiology, 2020
The analysis of the interaction between Helicobacter pylori (HP) and the host in vivo is an extremely informative way to enlighten the molecular mechanisms behind the persistency/latency of the bacterium as well as in the progression of the infection. An
Maria Felicia Soluri   +12 more
doaj   +1 more source

Functional interrogation of a SARS-CoV-2 host protein interactome identifies unique and shared coronavirus host factors

open access: yesCell Host and Microbe, 2020
The ongoing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has devastated the global economy and claimed more than 1.7 million lives, presenting an urgent global health crisis.
Hans-Heinrich Hoffmann   +20 more
semanticscholar   +1 more source

Gene co-expression in the interactome: moving from correlation toward causation via an integrated approach to disease module discovery

open access: yesnpj Systems Biology and Applications, 2021
In this study, we integrate the outcomes of co-expression network analysis with the human interactome network to predict novel putative disease genes and modules. We first apply the SWItch Miner (SWIM) methodology, which predicts important (switch) genes
P. Paci   +5 more
semanticscholar   +1 more source

Loss of AMBRA1 activates MAPK and angiogenesis signaling pathways in melanoma cells

open access: yesFEBS Open Bio, EarlyView.
Loss of AMBRA1 in melanoma cells activates multiple oncogenic pathways associated with tumor progression. Transcriptomic and protein network analyses revealed that AMBRA1 depletion enhances MAPK/ERK signaling, angiogenesis, TGF‐β/EMT signaling, and Wnt/axon guidance pathways.
Milad Ibrahim   +4 more
wiley   +1 more source

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