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Study · In silico · 2005

1 result

DNA double-helix binds regulatory peptides similarly to transcription factors.

Khavinson V, Shataeva L, Chernova A

Neuro endocrinology letters1 Jun 2005Cited by 10 (Europe PMC)

PMID15990728 (opens in a new tab)PepBankPUB-15990728
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study1

1 result from studies that gave the peptide. No result from this study comes from people.

  1. 01Computer modelIn silicoMechanism

    A complementary binding model predicted the base pair sequence ATTTTC as a specific binding site for the tetrapeptide epitalon, and this block was found repeatedly in the telomerase promoter region.

    In plain wordsIn a computer model, epitalon was predicted to bind the DNA sequence ATTTTC, which appears repeatedly in the promoter region of telomerase.

    Peptide
    Epitalon
    Outcome
    Not applicablePredicted DNA binding sequence of epitalon
    Study

    n: not reported in source

    complementary binding model of peptide and DNA
    Outcome group
    Receptor activity and mechanism · Pharmacology
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We have used complementary binding model to find a possible base pair sequence ATTTTC for specific binding of synthetic tetrapeptide epitalon. This base pair block and its reverse complement were found repeatedly in the promoter region of telomerase.

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

    10 Oct 2026, 08:19 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

Publication types

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