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Study · Measured the body's own peptide · 2001

2 results

Neutrophil-specific granule deficiency: homozygous recessive inheritance of a frameshift mutation in the gene encoding transcription factor CCAAT/enhancer binding protein--epsilon.

Gombart AF, Shiohara M, Kwok SH, Agematsu K, Komiyama A, Koeffler HP

Blood1 May 2001Cited by 102 (Europe PMC)

PMID11313242 (opens in a new tab)DOI10.1182/blood.v97.9.2561 (opens in a new tab)PepBankPUB-11313242
Publisher pagePubMedAsk about this study
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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 study2

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

Natural levels measured2

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. 01HumanEndogenous levelCase report or seriesOther

    In a patient with neutrophil-specific granule deficiency and a C/EBPepsilon mutation, mRNA for hCAP-18/LL‑37 was significantly lower.

    In plain wordsIn one patient with a rare neutrophil disorder, the body's own LL‑37 mRNA levels were lower.

    Peptide
    LL-37
    Outcome
    DecreasehCAP-18/LL-37 mRNA level in the patient with neutrophil-specific granule deficiency
    Study

    n = 1

    Outcome group
    Infection and antimicrobial activity · Immune and inflammation

    Source sentences

    Summary
    Consistent with this, a significant decrease in the levels of the messenger RNAs (mRNAs) encoding the secondary granule protein human 18-kd cationic antimicrobial protein (hCAP-18)/LL-37 and the primary granule protein bactericidal/permeability-increasing protein were observed in the patient.
    1 context sentence
    Summary · context
    To substantiate the role of C/EBPepsilon in the development of SGD and elucidate its mechanism of inheritance, the mutational status of the gene was determined in a second individual.

    This result measures the body's own LL-37. Nobody was given the peptide. It is not evidence about taking it.

  2. 02LabEndogenous levelIn vitro (cells)Mechanism

    In U937 cells, overexpression of C/EBPepsilon(32) induced hCAP-18 mRNA, the precursor of LL‑37.

    In plain wordsIn lab-grown leukemia cells, raising C/EBPepsilon increased mRNA for hCAP-18, the precursor of the body's own LL‑37.

    Peptide
    LL-37
    Outcome
    IncreasehCAP-18 mRNA induction by C/EBPepsilon overexpression
    Study

    humann: not reported in source

    U937 myeloid leukemia cell line
    Outcome group
    Infection and antimicrobial activity · Immune and inflammation

    Source sentences

    Summary
    The hCAP-18 mRNA was induced by overexpression of C/EBPepsilon(32) in the human myeloid leukemia cell line, U937, supporting the hypothesis that C/EBPepsilon is a key regulator of granule gene synthesis.

    This result measures the body's own LL-37. 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 3Current

    11 Oct 2026, 00:50 UTC

    Study results updated

  2. Version 2

    9 Oct 2026, 03:03 UTC

    Study data updated · source update from Europe PMC

  3. Version 1

    9 Oct 2026, 03:00 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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