Functional context for a residue

Usage

protvar_function(accession, position, ...)

Arguments

accession: A UniProt accession, for example "P04637".
position: A protein position. Use protvar_position() to get one out of a protein-change string.
...: Passed to biohttp::get_json(), for example throttle.

Value

A biohttp envelope whose data is a single string. See protvar_parse_function().

References

Stephenson et al. (2024). ProtVar: mapping and contextualizing human missense variation. Nucleic Acids Research 52(W1), W140-W147. doi:10.1093/nar/gkae413

Service documentation: https://www.ebi.ac.uk/ProtVar/

Examples

# \donttest{
biohttp::body_or_null(protvar_function("P04637", 175))
#> [1] "Multifunctional transcription factor that induces cell cycle arrest, DNA repair or apoptosis upon binding to its target DNA sequence. Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Negatively regulates cell division by controlling expression of a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. Its pro-apoptotic activity is activated via its interaction with PPP1R13B/ASPP1 or TP53BP2/ASPP2. However, this activity is inhibited when the interaction with PPP1R13B/ASPP1 or TP53BP2/ASPP2 is displaced by PPP1R13L/iASPP. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; the function is largely independent of transcription. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seems to have an effect on cell-cycle regulation. Implicated in Notch signaling cross-over. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Isoform 2 enhances the transactivation activity of isoform 1 from some but not all TP53-inducible promoters. Isoform 4 suppresses transactivation activity and impairs growth suppression mediated by isoform 1. Isoform 7 inhibits isoform 1-mediated apoptosis. Regulates the circadian clock by repressing CLOCK-BMAL1-mediated transcriptional activation of PER2"
# }