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Study · In vitro (cells) · 2012

5 results

Single-cell analyses reveal that KISS1R-expressing cells undergo sustained kisspeptin-induced signaling that is dependent upon an influx of extracellular Ca2+.

Babwah AV, Pampillo M, Min L, Kaiser UB, Bhattacharya M

Endocrinology15 Oct 2012Cited by 24 (Europe PMC)

PMID23070548 (opens in a new tab)PMCIDPMC3512071 (opens in a new tab)DOI10.1210/en.2012-1747 (opens in a new tab)PepBankPUB-23070548
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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 study5

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

  1. 01LabIn vitro (cells)Mechanism

    In HEK 293 cells, chronic kisspeptin‑10 treatment sustained activation of Gα(q/11), with prolonged phospholipase C and protein kinase C activation and intracellular Ca(2+) mobilization.

    In plain wordsIn human kidney cells grown in the lab, long kisspeptin‑10 treatment kept the receptor signal switched on for a long time.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseSustained Gαq/11 signaling in HEK 293 cells
    Study

    humann: not reported in source

    HEK 293 cells
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated · chronic treatmentAs given in this study (human).

    Source sentences

    Summary
    Through single-cell analyses, we tested our hypothesis in human embryonic kidney (HEK) 293 cells and found that was indeed the case.
    1 context sentence
    Summary · context
    chronic Kp-10 treatment would trigger the sustained activation of Gα(q/11) as evidenced through the prolonged activation of phospholipase C, protein kinase C, and prolonged mobilization of intracellular Ca(2+).
  2. 02LabIn vitro (cells)Mechanism

    Sustained KISS1R signaling also occurred in GT1-7 GnRH neuronal cells and Chinese hamster ovary cells, so it is likely a conserved property of KISS1R-expressing cells.

    In plain wordsIn lab-grown nerve cells and hamster ovary cells, the kisspeptin receptor also kept signaling for a long time.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseSustained KISS1R signaling in GT1-7 and CHO cells
    Study

    n: not reported in source

    GT1-7 GnRH neuronal and Chinese hamster ovary cell lines
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated · chronic treatmentAs given in this study.

    Source sentences

    Summary
    We subsequently determined that prolonged KISS1R signaling was not a phenomenon specific to HEK 293 cells but is likely a conserved property of KISS1R-expressing cells because evidence of sustained KISS1R signaling was also observed in the GT1-7 GnRH neuronal and Chinese hamster ovary cell lines.
    1 context sentence
    Summary · context
    chronic Kp-10 treatment would trigger the sustained activation of Gα(q/11) as evidenced through the prolonged activation of phospholipase C, protein kinase C, and prolonged mobilization of intracellular Ca(2+).
  3. 03LabIn vitro (cells)Mechanism

    Extracellular Ca(2+) was absolutely required to sustain chronic KISS1R signaling.

    In plain wordsIn lab cells, the long-lasting kisspeptin receptor signal needed calcium from outside the cell.

    Peptide
    Kisspeptin-10
    Outcome
    Not applicableRequirement of extracellular Ca(2+) for chronic KISS1R signaling
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    instead extracellular Ca(2+) was absolutely required for this.
    1 context sentence
    Summary · context
    chronic Kp-10 treatment would trigger the sustained activation of Gα(q/11) as evidenced through the prolonged activation of phospholipase C, protein kinase C, and prolonged mobilization of intracellular Ca(2+).
  4. 04LabIn vitro (cells)Mechanism

    Free intracellular Ca(2+), mainly from intracellular stores, was insufficient to sustain chronic KISS1R signaling.

    In plain wordsIn lab cells, calcium released from inside the cell was not enough to keep the receptor signal going.

    Peptide
    Kisspeptin-10
    Outcome
    No significant changeSufficiency of intracellular Ca(2+) for chronic KISS1R signaling
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We found that although free intracellular Ca(2+), primarily derived from intracellular stores, was sufficient to trigger the acute activation of a major KISS1R secondary effector, protein kinase C, it was insufficient to sustain chronic KISS1R signaling; instead extracellular Ca(2+) was absolutely required for this.
    1 context sentence
    Summary · context
    chronic Kp-10 treatment would trigger the sustained activation of Gα(q/11) as evidenced through the prolonged activation of phospholipase C, protein kinase C, and prolonged mobilization of intracellular Ca(2+).
  5. 05LabIn vitro (cells)Mechanism

    Free intracellular Ca(2+), mainly from intracellular stores, was sufficient to trigger acute activation of protein kinase C, a KISS1R secondary effector.

    In plain wordsIn lab cells, calcium from inside the cell was enough to start a short protein kinase C response.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseAcute protein kinase C activation by intracellular Ca(2+)
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We found that although free intracellular Ca(2+), primarily derived from intracellular stores, was sufficient to trigger the acute activation of a major KISS1R secondary effector, protein kinase C, it was insufficient to sustain chronic KISS1R signaling; instead extracellular Ca(2+) was absolutely required for this.
    1 context sentence
    Summary · context
    chronic Kp-10 treatment would trigger the sustained activation of Gα(q/11) as evidenced through the prolonged activation of phospholipase C, protein kinase C, and prolonged mobilization of intracellular Ca(2+).

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, 09:43 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:04 UTC

    First added · source update from Europe PMC

Subjects

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