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However, mRNAs do not move by themselves; instead they bind to a host of mRNA-binding proteins, and the ribosomes that are required for translation to take place.
To do this, PA must initially bind to a host cellular receptor.
To achieve this, the HIV virion must first bind to a host cell, primarily CD4+ T cells, macrophages and dendritic cells, and then 'hijack' their cellular machinery [ 5].
Collectively, these data indicate a host cell receptor with the capability of transmitting signal transduction in response to OipA; hence, it would be interesting to investigate whether recombinant OipA can bind to a host cell receptor and induce FAK signaling.
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The results indicate a convergent and complementary 1 1 binding mode, in which a BiPy ligand binds to a host molecule by ditopic ZnN coordination forming a stable cyclic supramolecular complex.
Once the human immunodeficiency virus (HIV) binds to a host immune cell through the interactions of the envelope protein with CD4 and a coreceptor, the host and virus membranes fuse and the HIV core, called the matrix/capsid, containing its RNA genome and related proteins enter the cell.
Mutations to hemagglutinin affect how well the protein binds to a host's cell surface receptor molecules, which determines how infective the virus strain is to the host organism.
For example, dimorphic fungal pathogen Blastomyces dermatitidis produces an adhesion molecule (BAD1) that binds to a host complement receptor in order to suppress production of pro-inflammatory cytokine TNF-α [34].
This is particularly true when an ectoparasite's life-cycle is entirely bound to a host individual resulting in co-speciation [e.g. [ 7- 10]].
The HIV Tat protein bound to a host super elongation complex (SEC) recognizes TAR and releases the paused polymerase (He et al., 2010; Sobhian et al., 2010).
A fascinating exception comes from recent experiments between E. coli B and λ-vir where an extensive arms race is only observed following the evolution of a 'key innovation' by the phage to bind to a new host receptor against which it has no history of prior adaptation (OmpF instead of LamB; Meyer et al., 2012).
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