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Study · Measured the body's own peptide · 2004

1 result

Mechanism of actin polymerization in cellular ATP depletion.

Atkinson SJ, Hosford MA, Molitoris BA

The Journal of biological chemistry17 Nov 2003Cited by 110 (Europe PMC)

Summary

Cellular ATP depletion in diverse cell types results in the net conversion of monomeric G-actin to polymeric F-actin and is an important aspect of cellular injury in tissue ischemia. We propose that this conversion results from altering the ratio of ATP-G-actin and ADP-G-actin, causing a net decrease in the concentration of thymosinactin complexes as a consequence of the differential affinity of thymosin beta4 for ATP- and ADP-G-actin. To test this hypothesis we examined the effect of ATP depletion induced by antimycin A and substrate depletion on actin polymerization, the nucleotide state of the monomer pool, and the association of actin monomers with thymosin and profilin in the kidney epithelial cell line LLC-PK1. ATP depletion for 30 min increased F-actin content to 145% of the levels under physiological conditions, accompanied by a corresponding decrease in G-actin content. Cytochalasin D treatment did not reduce F-actin formation during ATP depletion, indicating that it was predominantly not because of barbed end monomer addition. ATP-G-actin levels decreased rapidly during depletion, but there was no change in the concentration of ADP-G-actin monomers. The decrease in ATP-G-actin levels could be accounted for by dissociation of the thymosin-G-actin binary complex, resulting in a rise in the concentration of free thymosin beta4 from 4 to 11 microm. Increased detection of profilin-actin complexes during depletion indicated that profilin may participate in catalyzing nucleotide exchange during depletion. This mechanism provides a biochemical basis for the accumulation of F-actin aggregates in ischemic cells.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

No result from this study comes from a test of the peptide.

Natural levels measured1

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 01LabEndogenous levelIn vitro (cells)Mechanism

    In LLC-PK1 kidney epithelial cells, ATP depletion raised the concentration of free thymosin beta4 from 4 to 11 microm as thymosin-G-actin complexes dissociated.

    In plain wordsIn kidney cells under energy depletion, the body's own free thymosin beta4 rose as it came off actin.

    Outcome
    IncreaseFree thymosin beta4 concentration during ATP depletion
    Study

    n: not reported in source

    LLC-PK1 kidney epithelial cell line
    Outcome group
    Receptor activity and mechanism · Kidney and urinary

    Measurements

    Free thymosin beta4
    4 µM
    before ATP depletion
    Free thymosin beta4
    11 µM
    during ATP depletion

    Source sentences

    Summary
    The decrease in ATP-G-actin levels could be accounted for by dissociation of the thymosin-G-actin binary complex, resulting in a rise in the concentration of free thymosin beta4 from 4 to 11 microm.
    1 context sentence
    Summary · context
    To test this hypothesis we examined the effect of ATP depletion induced by antimycin A and substrate depletion on actin polymerization, the nucleotide state of the monomer pool, and the association of actin monomers with thymosin and profilin in the kidney epithelial cell line LLC-PK1.

    This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    13 Oct 2026, 01:52 UTC

    Study results updated

  2. Version 1

    12 Oct 2026, 18:17 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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