First-pass extracted concept

AP2-G V2163L mutation

Candidate: concept label1 source documents3 linked claims
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Aliases

AP2-G.L2163, single valine to leucine switch in AP2-G

Extracted Explainers

What the tool is doing

The paper presents the AP2-G V2163L variant as a loss-of-function mutation that disrupts DNA binding and sexual differentiation.

Source 1DOIPubMed

What problem it solves

It helps dissect which AP2-G residue is required for DNA binding and sexual commitment.

Source 1DOIPubMed

What it does not solve

The abstract does not present this mutant as a reusable engineering tool or therapeutic modality.

Source 1DOIPubMed

Alternatives

The abstract contrasts AP2-G.L2163 with AP2-G.V2163, the functional wild-type residue state.

Source 1DOIPubMed

Evidence Snippets

We discovered a single valine(V2163) to leucine(L2163) mutation in a transcription factor required for P. falciparum gametocytogenesis (AP2-G) that abrogates sexual differentiation.
Evidence 1Source 1DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1functional effectsupports2026Source 1DOIPubMed

The AP2-G V2163L mutation abrogates sexual differentiation in Plasmodium falciparum.

Quoted textsource-backed
We discovered a single valine(V2163) to leucine(L2163) mutation in a transcription factor required for P. falciparum gametocytogenesis (AP2-G) that abrogates sexual differentiation.
Claim 2mechanismsupports2026Source 1DOIPubMed

AP2-G.L2163 does not bind the ap2-g consensus motif GnGTAC and does not stimulate gene transcription including autoregulation.

Quoted textsource-backed
AP2-G.L2163 does not bind the ap2-g consensus motif, GnGTAC, or stimulate gene transcription, including autoregulation.
Claim 3structure functionsupports2026Source 1DOIPubMed

Residue V2163 in AP2-G plays a critical role in DNA binding.

Quoted textsource-backed
Together this work demonstrates that V2163 in AP2-G plays a critical role in DNA binding