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The molecular mechanisms N. meningitidis employ to manipulate the immune system, translocate the mucosal Human-associated bacteria encode a variety of bioactive small molecules with growing evidence for N-acyl Here, we heterologously expressed an N-acyltransferase encoded in the obligate human pathogen N. meningitidis and identified 30 N-acyl amides with representative members serving as agonists of the G-protein coupled During this process, we also characterized two mammalian N-acyl amides derived from the bovine medium

October 2022 N-terminal alterations turn the gut hormone GLP-2 into an antagonist with gradual loss of Searching for antagonist activity, we performed systematic N-terminal truncations of human GLP-2(1-33

September 2022 Isoforms of GPR35 have distinct extracellular N-termini that allosterically modify receptor-transducer known to be expressed as two distinct isoforms that differ only in the length of their extracellular N-termini Our results reveal that the extended N-terminus of the long isoform limits G protein activation yet elevates We found that a proposed disulfide bridge between the N-terminus and extracellular loop 3, present in is crucial for constitutive G13 activation, while an additional cysteine contributed by the extended N-terminus

Kar-Ming Fung , Chao Xu , Resham Bhattacharya , Priyabrata Mukherjee , Ciro Isidoro , Yong Sang Song , Danny N Dhanasekaran Tags GPCR , High Grade Serous Ovarian Carcinoma , Let-7 miRNAs , Oncogenic Pathways ,

< GPCR News < GPCRs in Oncology and Immunology Chemokine N-terminal-derived peptides differentially regulate MIP chemokines, such as CCL3 and CCL5 are processed at the N-terminus, which influences signaling in Here, we investigate the signaling capacity of peptides corresponding to truncated N-termini. In conclusion, chemokine N-termini can be mimicked to produce small CCR1-selective agonists, as well

therapy relapse and impact of different salvage strategies in an international cohort of 139 patients (n = 130 ide-cel, n = 9 cilta-cel), receiving talquetamab (n = 28), teclistamab (n = 37), combinations of immunomodulating drugs (IMiDs), proteasome inhibitors (PIs) or CD38 monoclonal antibodies (n = 43), and others (n = 31). Authors Maximilian Merz, Danai Dima, Hamza Hashmi, Nausheen Ahmed, Friedrich Stölzel, Tobias A W Holderried