Binding of an N-ethylmaleimide-sensitive fusion protein to Golgi membranes requires both a soluble protein(s) and an integral membrane receptor. [PDF]
, 1989 P J Weidman +3 more
openalex +1 more source
Molecular Oncology, EarlyView.This study indicates that Merkel cell carcinoma (MCC) does not originate from Merkel cells, and identifies gene, protein & cellular expression of immune‐linked and neuroendocrine markers in primary and metastatic Merkel cell carcinoma (MCC) tumor samples, linked to Merkel cell polyomavirus (MCPyV) status, with enrichment of B‐cell and other immune cell
Richie Jeremian +10 more
wiley +1 more source
Epstein-Barr virus latent membrane protein-1 oncogene deletions: correlations with malignancy in Epstein-Barr virus--associated lymphoproliferative disorders and malignant lymphomas [PDF]
, 1996 DW Kingma +5 more
openalex +1 more source
YAP1::TFE3 mediates endothelial‐to‐mesenchymal plasticity in epithelioid hemangioendothelioma
Molecular Oncology, EarlyView.The YAP1::TFE3 fusion protein drives endothelial‐to‐mesenchymal transition (EndMT) plasticity, resulting in the loss of endothelial characteristics and gain of mesenchymal‐like properties, including resistance to anoikis, increased migratory capacity, and loss of contact growth inhibition in endothelial cells.
Ant Murphy +9 more
wiley +1 more source
Quantifying Protein-Protein Interactions of Peripheral Membrane Proteins by Fluorescence Brightness Analysis [PDF]
, 2014 Elizabeth M. Smith +3 more
openalex +1 more source
Emerging role of ARHGAP29 in melanoma cell phenotype switching
Molecular Oncology, EarlyView.This study gives first insights into the role of ARHGAP29 in malignant melanoma. ARHGAP29 was revealed to be connected to tumor cell plasticity, promoting a mesenchymal‐like, invasive phenotype and driving tumor progression. Further, it modulates cell spreading by influencing RhoA/ROCK signaling and affects SMAD2 activity. Rho GTPase‐activating protein
Beatrice Charlotte Tröster +3 more
wiley +1 more source
Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine
Molecular Oncology, EarlyView.The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu +18 more
wiley +1 more source
Quantitation of the loss of the bacteriophage lambda receptor protein from the outer membrane of lipopolysaccharide-deficient strains of Escherichia coli [PDF]
, 1975 Linda L. Randall
openalex +1 more source
A synthetic benzoxazine dimer derivative targets c‐Myc to inhibit colorectal cancer progression
Molecular Oncology, EarlyView.Benzoxazine dimer derivatives bind to the bHLH‐LZ region of c‐Myc, disrupting c‐Myc/MAX complexes, which are evaluated from SAR analysis. This increases ubiquitination and reduces cellular c‐Myc. Impairing DNA repair mechanisms is shown through proteomic analysis.
Nicharat Sriratanasak +8 more
wiley +1 more source
Frontiers in Cellular and Infection MicrobiologyHost iron deficiency is protective against severe malaria as the human malaria parasite Plasmodium falciparum depends on bioavailable iron from its host to proliferate.
Juliane Wunderlich +8 more
doaj +1 more source