Results 131 to 140 of about 869,886 (263)

Navigating risk in biological quality testing: A guide for emerging laboratories. [PDF]

open access: yesIndian J Med Res
Shrivastava R   +4 more
europepmc   +1 more source

Structural studies and functional engineering of NanX: an anhydro‐sialic acid transporter from Escherichia coli

open access: yesFEBS Open Bio, EarlyView.
Biophysical characterisation shows that NanX, a membrane transport protein from the major facilitator superfamily (MFS), forms both monomers and dimers after purification. AlphaFold modelling and substrate docking provide information on residues likely involved in substrate recognition for NanX and another MFS member, NanT.
Michael C. Newton‐Vesty   +13 more
wiley   +1 more source

Avidin is evolutionarily conserved in fish but dispensable for development and resistance against Streptococcus agalactiae in zebrafish

open access: yesFEBS Open Bio, EarlyView.
The presence of biotin‐binding avidin proteins in fish and their biological significance are poorly characterized. We cataloged fish avidins and demonstrate that they are widely present and evolutionarily conserved. We created avd knockout zebrafish and show that zebavidin is dispensable for development and that resistance of avd knockout embryos in ...
Anni K. Saralahti   +5 more
wiley   +1 more source

Aging Is a Key Driver for Adult Acute Myeloid Leukemia

open access: yesAging and Cancer, EarlyView.
Acute myeloid leukemia (AML) is a classical age‐related hematologic malignancy, and a key driver of AML is aging, which profoundly regulates intrinsic factors such as genomic instability, epigenetic reprogramming, and metabolic dysregulation, and alters bone marrow microenvironment.
Rong Yin, Haojian Zhang
wiley   +1 more source

Mutant NPM1 in Acute Myeloid Leukemia Initiation and Maintenance

open access: yesAging and Cancer, EarlyView.
NPM1 mutations drive acute myeloid leukemia by acting as neomorphic transcriptional regulators that cooperate with Menin–MLL and XPO1 to sustain HOX/MEIS1 expression and block differentiation. Targeting these mutant‐specific transcriptional dependencies provides a rational therapeutic strategy for NPM1‐mutated AML.
Yanan Jiang   +3 more
wiley   +1 more source

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