Results 61 to 70 of about 1,268,660 (340)

Organoids in pediatric cancer research

open access: yesFEBS Letters, EarlyView.
Organoid technology has revolutionized cancer research, yet its application in pediatric oncology remains limited. Recent advances have enabled the development of pediatric tumor organoids, offering new insights into disease biology, treatment response, and interactions with the tumor microenvironment.
Carla Ríos Arceo, Jarno Drost
wiley   +1 more source

PICMI: mapping point mutations on genomes [PDF]

open access: yesBioinformatics, 2010
Abstract Motivation: Several international collaborations and local projects are producing extensive catalogues of genomic variations that are supplementing existing collections such as the OMIM catalogue. The flood of this type of data will keep increasing and, especially, it will be relevant to a wider user base, including not only ...
LE PERA, LOREDANA   +2 more
openaire   +4 more sources

Reciprocal control of viral infection and phosphoinositide dynamics

open access: yesFEBS Letters, EarlyView.
Phosphoinositides, although scarce, regulate key cellular processes, including membrane dynamics and signaling. Viruses exploit these lipids to support their entry, replication, assembly, and egress. The central role of phosphoinositides in infection highlights phosphoinositide metabolism as a promising antiviral target.
Marie Déborah Bancilhon, Bruno Mesmin
wiley   +1 more source

Helical ambivalency induced by point mutations [PDF]

open access: yesBMC Structural Biology, 2013
Mutation of amino acid sequences in a protein may have diverse effects on its structure and function. Point mutations of even a single amino acid residue in the helices of the non-redundant database may lead to sequentially identical peptides which adopt different secondary structures in different proteins.
Bhattacharjee, Nicholus, Biswas, Parbati
openaire   +2 more sources

Spatiotemporal and quantitative analyses of phosphoinositides – fluorescent probe—and mass spectrometry‐based approaches

open access: yesFEBS Letters, EarlyView.
Fluorescent probes allow dynamic visualization of phosphoinositides in living cells (left), whereas mass spectrometry provides high‐sensitivity, isomer‐resolved quantitation (right). Their synergistic use captures complementary aspects of lipid signaling. This review illustrates how these approaches reveal the spatiotemporal regulation and quantitative
Hiroaki Kajiho   +3 more
wiley   +1 more source

Molecular dynamics approach to the I431V mutational impact on thyroid hormone receptor-beta

open access: yesBibechana, 2018
The point mutations like I431V on thyroid hormone receptor-beta (THR-β) gene cause resistance to thyroid hormones (RTH) with the clinical diagnosis of elevated free triiodothyronine (T3) and free thyroxin (T4) but not suppressed thyroid stimulating ...
Tika Ram Lamichhane   +3 more
doaj   +3 more sources

An intracellular transporter mitigates the CO2‐induced decline in iron content in Arabidopsis shoots

open access: yesFEBS Letters, EarlyView.
This study identifies a gene encoding a transmembrane protein, MIC, which contributes to the reduction of shoot Fe content observed in plants under elevated CO2. MIC is a putative Fe transporter localized to the Golgi and endosomal compartments. Its post‐translational regulation in roots may represent a potential target for improving plant nutrition ...
Timothy Mozzanino   +7 more
wiley   +1 more source

Sequence analysis of bla CTX-M-28 , an ESBL responsible for third-generation cephalosporin resistance in Enterobacteriaceae, for the first time in India

open access: yesIndian Journal of Pathology and Microbiology, 2008
The most common group of ESBLs not belonging to the bla TEM or bla SHV families were termed bla CTX-M , to highlight their ESBLs′ greater activity against cefotaxime than against ceftazidime.
Kingsley Jemima, Verghese Susan
doaj  

Mitochondrial damage and senescence phenotype of cells derived from a novel frataxin G127V point mutation mouse model of Friedreich's ataxia

open access: yesDisease Models & Mechanisms, 2020
Friedreich's ataxia (FRDA) is an autosomal recessive neurodegenerative disease caused by reduced expression of the mitochondrial protein frataxin (FXN).
Daniel Fil   +9 more
doaj   +1 more source

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