Publications by authors named "J I Hopkins"

Time-resolved small-angle X-ray experiments are reported here that capture and quantify a previously unknown rapid collapse of the unfolded oligonucleotide as an early step in the folding of hybrid 1 and hybrid 2 telomeric G-quadruplex structures. The rapid collapse, initiated by a pH jump, is characterized by an exponential decrease in the radius of gyration from 24.3 to 12.

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MAPK signaling activation is an important driver event in colorectal cancer (CRC) tumorigenesis that informs therapy selection, but detection by liquid biopsy can be challenging. We analyze real-world comprehensive genomic profiling (CGP) data to explore the landscape of alterations in BRAF or RAS in CRC patients (N = 51 982) and co-occurrence with other biomarkers. A pathogenic RAS or BRAF alteration was found in 63.

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Forty percent of terrestrial ecosystems require recurrent fires driven by feedbacks between fire and plant fuels. The accumulation of fine fuels in these ecosystems play a key role in fire intensity, which alters soil nutrients and shapes soil microbial and plant community responses to fire. Changes to post-fire plant fuel production are well known to feed back to future fires, but post-fire decomposition of new fuels is poorly understood.

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The host enzyme heparanase (HPSE) facilitates the release of herpes simplex virus type 2 (HSV-2) from target cells by cleaving the viral attachment receptor heparan sulfate (HS) from infected cell surfaces. HPSE 2, an isoform of HPSE, binds to but does not possess the enzymatic activity needed to cleave cell surface HS. Our study demonstrates that HSV-2 infection significantly elevates HPSE 2 protein levels, impacting two distinct stages of viral replication.

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The T cell antigen presentation platform MR1 consists of 6 allomorphs in humans that differ by no more than 5 amino acids. The principal function of this highly conserved molecule involves presenting microbial metabolites to the abundant mucosal-associated invariant T (MAIT) cell subset. Recent developments suggest that the role of MR1 extends to presenting antigens from cancer cells, a function dependent on the K43 residue in the MR1 antigen binding cleft.

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