What they found

Comprehensive review/research article from the Carlier lab (MF Carlier is the authoritative actin dynamics biochemist) on the β-thymosin/WH2 module. Used chimeric protein engineering, actin polymerization assays, ITC, NMR, and SAXS to dissect how a single βT/WH2 domain can function as G-actin sequesterer, filament barbed-end deliverer, nucleator, or severer depending on C-terminal sequence context.

Numbers that matter

Thymosin-β4 (Tβ4) × G-actin:

  • Kd = 1 μM for ATP-actin (moderate affinity, the reference baseline)
  • Kd = 80–100 μM for ADP-actin (50–100× weaker — nucleotide-state dependent)

Tβ4 × F-actin (side-binding):

  • Kd = 5–10 mM (weak cooperative binding at [Tβ4] > 20 μM)
  • This is 5,000–10,000× weaker than G-actin binding
  • Mechanism: C-terminal α-helix of Tβ4 interferes with filament contacts

Implication for WH2 × F-actin:

  • WH2 lacks the C-terminal α-helix that interferes with F-actin in Tβ4
  • But WH2 canonical binding site (barbed-end groove) is also involved in longitudinal actin–actin contacts in filament — still not a clean side-binding site
  • No direct measurement of WH2 × F-actin Kd reported in this paper
  • The paper does not support the existence of a low-μM WH2 × F-actin interaction

Context for model parameter WH2_KD_FACTIN_M = 5 μM:

  • Based on all available literature, 5 μM would be VERY optimistic for a WH2 × F-actin side-binding event. It is possible if constructs are specifically engineered, but not for a canonical isolated WH2 peptide. True value is likely ≥ 1 mM or unmeasurable.

Connections