Results 31 to 40 of about 113 (110)

Thermostable neutral metalloprotease from Geobacillus sp. EA1 does not share thermolysin's preference for substrates with leucine at the P1′ position

open access: yesFEBS Letters, EarlyView.
Knowing how proteases recognise preferred substrates facilitates matching proteases to applications. The S1′ pocket of protease EA1 directs cleavage to the N‐terminal side of hydrophobic residues, particularly leucine. The S1′ pocket of thermolysin differs from EA's at only one position (leucine in place of phenylalanine), which decreases cleavage ...
Grant R. Broomfield   +3 more
wiley   +1 more source

Operator inequalities associated with Hölder–McCarthy and Kantorovich inequalities

open access: yesJournal of Inequalities and Applications, 1998
We discuss operator inequalities associated with Hölder–McCarthy and Kantorovich inequalities. We give a complementary inequality of Hölder–McCarthy one as an extension of [2] and also we give an application to the order preserving power inequality.
openaire   +1 more source

Redox‐dependent binding and conformational equilibria govern the fluorescence decay of NAD(P)H in living cells

open access: yesFEBS Letters, EarlyView.
In this work, we reveal how different enzyme binding configurations influence the fluorescence decay of NAD(P)H in live cells using time‐resolved anisotropy imaging and fluorescence lifetime imaging microscopy (FLIM). Mathematical modelling shows that the redox states of the NAD and NADP pools govern these configurations, shaping their fluorescence ...
Thomas S. Blacker   +8 more
wiley   +1 more source

Neutrophil deficiency increases T cell numbers at the site of tissue injury in mice

open access: yesFEBS Letters, EarlyView.
In wild‐type mice, injury or acute inflammation induces neutrophil influx followed by macrophage accumulation. Mcl1ΔMyelo (neutrophil‐deficient) mice lack neutrophils, and in response to muscle injury show fewer macrophages and exhibit strikingly elevated T‐cell numbers, primarily non‐conventional “double‐negative” (DN) αβ and γδ T cells.
Hajnalka Halász   +6 more
wiley   +1 more source

Development of visible light‐sensitive human neuropsin (OPN5) via single amino acid substitution

open access: yesFEBS Letters, EarlyView.
The present study determines a key amino acid residue, Lys91, for defining UV sensitivity of human OPN5. Heterologous action spectroscopy of the wild type and K91 mutants of OPN5 in HEK293T cells reveals that substitution of Lys91 with neutral (alanine) or acidic amino acids (glutamic or aspartic acids) causes substantial shifts in spectral sensitivity
Yusuke Sakai   +2 more
wiley   +1 more source

A Note on Hölder Type Inequality for the Fermionic p-Adic Invariant q-Integral

open access: yesJournal of Inequalities and Applications, 2009
The purpose of this paper is to find Hölder type inequality for the fermionic p-adic invariant q-integral which was defined by Kim (2008).
openaire   +2 more sources

C‐mannosylation promotes ADAMTS1 activation and secretion in human testicular germ cell tumor NEC8 cells

open access: yesFEBS Letters, EarlyView.
C‐mannosylation is a unique form of protein glycosylation. In this study, we demonstrated that ADAMTS1 is C‐mannosylated at Trp562 and Trp565 in human testicular germ cell tumor NEC8 cells. We found that C‐mannosylation of ADAMTS1 is essential for its secretion, processing, enzymatic activity, and ability to promote vasculogenic mimicry. These findings
Takato Kobayashi   +5 more
wiley   +1 more source

The multidrug and toxin extrusion (MATE) transporter DTX51 antagonizes non‐cell‐autonomous HLS1–AMP1 signaling in a region‐specific manner

open access: yesFEBS Letters, EarlyView.
The Arabidopsis mutants hls1 hlh1 and amp1 lamp1 exhibit pleiotropic developmental phenotypes. Although the functions of the causative genes remain unclear, they act in the same genetic pathway and are thought to generate non‐cell‐autonomous signals.
Takashi Nobusawa, Makoto Kusaba
wiley   +1 more source

Ergothioneine supplementation improves pup phenotype and survival in a murine model of spinal muscular atrophy

open access: yesFEBS Letters, EarlyView.
Spinal muscular atrophy (SMA) is a genetic disease affecting motor neurons. Individuals with SMA experience mitochondrial dysfunction and oxidative stress. The aim of the study was to investigate the effect of an antioxidant and neuroprotective substance, ergothioneine (ERGO), on an SMNΔ7 mouse model of SMA.
Francesca Cadile   +8 more
wiley   +1 more source

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