Synthetic peptide TEKKRRETVEREKE derived from ezrin induces differentiation of NIH/3T3 fibroblasts.

Chulkina M, Negmadjanov U, Lebedeva E, Pichugin A, Mazurov D, Ataullakhanov R, Holmuhamedov E

European journal of pharmacology28 Jun 2017Cited by 1 (Europe PMC)

PMID28668507DOI10.1016/j.ejphar.2017.06.033PepBankPUB-28668507

Publisher page PubMedAsk about this study

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 study6

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

01LabIn vitro (cells)Mechanism
In NIH/3T3 fibroblasts, Gepon induced morphological and biochemical changes characteristic of differentiated fibroblasts.
In plain wordsIn cells, Gepon induced shape and biochemical changes characteristic of differentiated fibroblasts.
Peptide
Gepon
Outcome
Not applicableFibroblast morphological and biochemical differentiation
Study
mousen: not reported in source
NIH/3T3 embryonic mouse fibroblasts
Outcome group
Receptor activity and mechanism · Skin and wound
Studied dose
Dose not stated
Source sentences
Summary
Gepon treatment of NIH/3T3 cells resulted in morphological and biochemical changes, characteristic of differentiated fibroblasts.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of current study was to investigate intracellular signaling pathways involved in the effect of this peptide on wild type and genetically modified (CD44 KO) NIH/3T3 embryonic mouse fibroblasts.
Report a problemFND-2866850701
02LabIn vitro (cells)Mechanism
In NIH/3T3 fibroblasts, Gepon activated only ERK1/2-dependent signaling, whereas TGF-β1 activated canonical and non-canonical pathways.
In plain wordsIn cells, Gepon activated only ERK-dependent signaling, whereas TGF-β1 activated canonical and non-canonical pathways.
Peptide
Gepon
Outcome
Not applicableERK1/2-dependent signaling activation
Study
mousen: not reported in source
NIH/3T3 embryonic mouse fibroblasts
Comparator
TGF-β1
Outcome group
Receptor activity and mechanism · Skin and wound
Studied dose
Dose not stated
Source sentences
Summary
While treatment of NIH/3T3 cells with TGF-β1 triggered the activation of both canonical and non-canonical signaling pathways, exposure of fibroblasts to Gepon activated only the ERK1/2 dependent pathway without modulating SMAD dependent signaling pathway.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of current study was to investigate intracellular signaling pathways involved in the effect of this peptide on wild type and genetically modified (CD44 KO) NIH/3T3 embryonic mouse fibroblasts.
Report a problemFND-2866850702
03LabIn vitro (cells)Mechanism
In NIH/3T3 fibroblasts, Gepon did not modulate SMAD-dependent signaling.
In plain wordsIn cells, Gepon did not change SMAD-dependent signaling in fibroblasts.
Peptide
Gepon
Outcome
No significant changeSMAD-dependent signaling
Study
mousen: not reported in source
NIH/3T3 embryonic mouse fibroblasts
Outcome group
Receptor activity and mechanism · Skin and wound
Studied dose
Dose not stated
Source sentences
Summary
While treatment of NIH/3T3 cells with TGF-β1 triggered the activation of both canonical and non-canonical signaling pathways, exposure of fibroblasts to Gepon activated only the ERK1/2 dependent pathway without modulating SMAD dependent signaling pathway.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of current study was to investigate intracellular signaling pathways involved in the effect of this peptide on wild type and genetically modified (CD44 KO) NIH/3T3 embryonic mouse fibroblasts.
Report a problemFND-2866850703
04LabIn vitro (cells)Mechanism
In NIH/3T3 fibroblasts, Gepon increased formation of alpha-SMA-containing stress filaments independently of CD44 receptor presence.
In plain wordsIn cells, Gepon increased formation of alpha-SMA-containing stress filaments with or without the CD44 receptor.
Peptide
Gepon
Outcome
IncreaseAlpha-SMA-containing stress filament formation
Study
mousen: not reported in source
NIH/3T3 embryonic mouse fibroblasts
Outcome group
Receptor activity and mechanism · Skin and wound
Studied dose
Dose not stated
Source sentences
Summary
Activation of the MAPK signaling pathway and the increase in formation of α-SMA containing stress filaments induced by Gepon were independent on presence of CD44 receptor in NIH/3T3 fibroblasts.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of current study was to investigate intracellular signaling pathways involved in the effect of this peptide on wild type and genetically modified (CD44 KO) NIH/3T3 embryonic mouse fibroblasts.
Report a problemFND-2866850706

Studies that did not test the peptide alone2

In this study, Gepon was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Gepon.

05LabNot a test of Gepon aloneIn vitro (cells)Mechanism
In NIH/3T3 fibroblasts, CD44 knockout did not change Gepon-dependent activation of intracellular signaling pathways.
In plain wordsIn cells, removal of the CD44 gene did not change Gepon-dependent signaling compared with fibroblasts with CD44.
Peptide
Gepon
Outcome
No significant changeCD44 dependence of Gepon signaling
Study
mousen: not reported in source
NIH/3T3 embryonic mouse fibroblasts
Comparator
Fibroblasts with CD44 receptor
Outcome group
Receptor activity and mechanism · Skin and wound
Source sentences
Summary
Knocking out hyaluronic acid CD44 receptor did not change Gepon or TGF-β1 dependent activation of intracellular signaling pathways and assembling of α-SMA-positive filaments.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of current study was to investigate intracellular signaling pathways involved in the effect of this peptide on wild type and genetically modified (CD44 KO) NIH/3T3 embryonic mouse fibroblasts.
In this study, Gepon was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Gepon.
Report a problemFND-2866850704
06LabNot a test of Gepon aloneIn vitro (cells)Mechanism
In NIH/3T3 fibroblasts, CD44 knockout did not change Gepon-dependent assembly of alpha-SMA-positive filaments.
In plain wordsIn cells, removal of the CD44 gene did not change Gepon-dependent filament assembly compared with fibroblasts with CD44.
Peptide
Gepon
Outcome
No significant changeCD44 dependence of alpha-SMA filament assembly
Study
mousen: not reported in source
NIH/3T3 embryonic mouse fibroblasts
Comparator
Fibroblasts with CD44 receptor
Outcome group
Receptor activity and mechanism · Skin and wound
Source sentences
Summary
Knocking out hyaluronic acid CD44 receptor did not change Gepon or TGF-β1 dependent activation of intracellular signaling pathways and assembling of α-SMA-positive filaments.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of current study was to investigate intracellular signaling pathways involved in the effect of this peptide on wild type and genetically modified (CD44 KO) NIH/3T3 embryonic mouse fibroblasts.
In this study, Gepon was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Gepon.
Report a problemFND-2866850705

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.

Version 2Current
27 Oct 2026, 18:20 UTC
Study results updated
Version 1
27 Oct 2026, 16:32 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

PepBank is a research reference. Talk to a doctor before you use any peptide.