Scientifically reviewed by
Dr. Ky H. Le, MD
The information presented in this article is for educational and research purposes only, intended for laboratory professionals, researchers and collaborators. This content does not constitute medical or clinical advice.
Research into bioregulatory peptides has revealed compounds that work through direct interaction with cellular DNA. Cartalax represents one such peptide with tissue-specific effects on aging and regeneration.
The compound’s structural similarity to collagen sequences allows it to influence gene expression patterns in connective tissues. This makes it a valuable tool for studying cellular aging mechanisms in controlled laboratory settings.
Key Research Insights
- Cartalax is a tripeptide bioregulator with a sequence similar to type XI collagen that targets connective tissue cells.
- The peptide reduces key aging markers like p16, p21, and p53 while increasing SIRT6, a protein linked to longevity.
- Research demonstrates effects on fibroblast proliferation, cartilage regeneration, and kidney cell renewal.
- Laboratory applications focus on cellular senescence, extracellular matrix biology, and tissue-specific aging pathways.
What is Cartalax?
Cartalax is a synthetic tripeptide consisting of alanine, glutamic acid, and aspartic acid (AED sequence). This specific arrangement matches sequences found in the alpha-1 chain of type XI collagen.
Type XI collagen plays a key role in maintaining cartilage integrity and organizing the extracellular matrix. The peptide’s structural similarity to this collagen component explains its tissue-specific effects.
| Property | Description |
|---|---|
| Sequence | Ala-Glu-Asp (AED) |
| Structural Origin | Type XI collagen alpha-1 chain |
| Classification | Bioregulatory tripeptide |
| Primary Targets | Connective tissue, fibroblasts, chondrocytes |
Cartalax emerged from Russian peptide research focused on organ-specific bioregulators. These short peptides operate through epigenetic mechanisms rather than traditional receptor signaling.
The peptide binds directly to specific DNA sequences in cell nuclei. This interaction modulates gene expression patterns involved in aging and tissue repair.
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How Cartalax Works at the Cellular Level
Cartalax functions as a cytogenetic peptide that binds to regulatory DNA sequences. This binding alters gene expression in tissue-specific patterns.
The peptide guides transcription toward restoration of physiological balance. It enhances synthesis of structural proteins while suppressing catabolic pathways.
This mechanism differs from traditional pharmacological agents. Rather than activating cell surface receptors, Cartalax works directly at the nuclear level.
Gene Expression Modulation
Research shows Cartalax affects numerous genes involved in aging processes. Expression changes range from 1.6-fold to 5.6-fold for genes including IGF1, FOXO1, TERT, TNKS2, and NF-kB[1].
These dramatic shifts suggest the peptide can reset aging cells to a more youthful expression pattern. The breadth of effects indicates comprehensive impact on cellular aging pathways.
The peptide’s small size allows it to enter cells and reach nuclear targets. Once bound to DNA, it influences which genes get transcribed and at what levels.
SIRT6 and p53 Interactions
Cartalax increases expression of SIRT6, a sirtuin protein strongly linked to longevity and genomic stability. Low SIRT6 levels trigger cellular senescence, making this upregulation significant.
The relationship between SIRT6 and p53 involves complex cooperation. Research demonstrates that p53 can recruit SIRT6 to chromatin where they work together to regulate cellular functions[2].
SIRT6 acts as a co-activator of p53, recruiting RNA polymerase II to specific promoters. This enhances gene expression in coordinated aging responses.
Cartalax influences both proteins simultaneously. It increases SIRT6 while decreasing p53, creating a balance that favors cellular longevity over senescence.
Related Product: Buy Cartalax for laboratory research use.
The Research Behind Cartalax Bioregulator
Laboratory investigations into Cartalax cover multiple tissue types and cellular processes. The following sections detail key findings organized by research area and mechanism.
Cellular Aging and Senescence
Cartalax demonstrates clear effects on cellular aging pathways through modulation of senescence markers. Renal epithelial cell cultures show decreased expression of p16, p21, and p53 proteins[3].
These proteins form core components of cellular senescence machinery. p53 serves as a tumor suppressor and pro-apoptotic transcription factor that increases during aging.
The peptide’s ability to reduce p53 signaling suggests a mechanism for delaying senescence. This prevents premature cell death pathways that contribute to tissue aging.
SIRT6 upregulation by Cartalax represents another key finding. This protein correlates strongly with longevity and genomic stability across species.
The bidirectional relationship between SIRT6 and p53 adds complexity to these effects. Their cooperation in chromatin regulation creates sophisticated control over aging responses.
Fibroblast Function and Proliferation
Fibroblasts are ubiquitous connective tissue cells found throughout cartilage, skin, blood vessels, and kidneys. Cartalax exerts multiple effects on fibroblast biology.
The peptide increases Ki-67 expression, a widely recognized marker of cell proliferation. This enhancement proves particularly significant in aging fibroblast cultures where Ki-67 typically decreases[4].
Cartalax also increases CD98hc, a glycoprotein involved in cellular regeneration and aging processes. This upregulation helps maintain regenerative capacity as cells age.
Anti-apoptotic properties appear through suppressed caspase-3 activity. Caspase-3 executes programmed cell death, so its inhibition allows fibroblasts to avoid age-related death.
Key fibroblast effects include:
- Enhanced proliferation through Ki-67 upregulation
- Increased CD98hc expression supporting regeneration
- Reduced caspase-3 activity preventing apoptosis
- Maintained cellular vitality in aging cultures
Extracellular Matrix Effects
Cartalax influences extracellular matrix remodeling through inhibition of matrix metalloproteinase-9 (MMP-9) synthesis. MMP-9 degrades ECM components, with activity increasing during aging[4].
By inhibiting MMP-9, the peptide preserves matrix integrity. This prevents degenerative changes typically seen with advancing cellular age.
Matrix preservation maintains tissue structural stability. The ECM provides scaffolding for cells and regulates their behavior through biochemical signals.
Research shows these effects prove crucial for connective tissue health. Maintaining ECM integrity supports proper cellular function and tissue organization.
Cartilage and Chondrocyte Research
Chondrocytes are specialized cells responsible for maintaining cartilage matrix. Laboratory work using rat cartilage tissue cultures reveals specific Cartalax effects.
The peptide increases cartilage area index by 18-38% in cultures from both young and old specimens. This indicates enhanced growth and regeneration capacity.
Mechanisms involve increased chondrocyte proliferation and enhanced formation of new cartilage tissue. These effects occur around original tissue fragments in culture systems.
Cartalax stimulates proliferating cell nuclear antigen (PCNA), a molecular marker of chondrocyte proliferation and growth. Simultaneously, it reduces p53 protein synthesis.
This dual action of promoting proliferation while preventing apoptosis creates conditions favorable for cartilage regeneration. The balance between growth and cell death shifts toward tissue maintenance.
The peptide may also stimulate synthesis of extracellular matrix components. These include proteoglycans and collagen type II, both essential for cartilage resilience and elasticity.
Kidney Function and Renal Research
Early Cartalax research originated from studies using polypeptide isolates from calf kidneys. These isolates stimulated cell renewal in older rat kidneys.
The compounds increased Ki-67 while decreasing p53 levels. Chemical analysis revealed Cartalax as one of the active components responsible for these effects.
Renal cell culture studies confirm direct effects. The peptide increases cell proliferation while decreasing multiple aging markers including p16, p21, and p53[3].
These proteins constitute fundamental senescence pathway components. Their reduction suggests Cartalax helps maintain kidney cell function and vitality.
The effects prove particularly significant given that kidney function naturally declines with age. Susceptibility to chronic conditions increases as renal cells lose regenerative capacity.
Current Research Gaps and Future Directions
Despite documented effects, Cartalax research remains limited compared to other peptide bioregulators. Most available studies examine broad peptide categories rather than individual compounds.
The precise molecular interactions need deeper investigation. While we know Cartalax affects chromatin structure and gene expression, the exact binding sites remain unclear.
Questions researchers are exploring:
- Which specific DNA sequences does Cartalax bind in different cell types?
- How does the peptide’s structure determine its tissue selectivity?
- What determines the duration of epigenetic changes it produces?
- Can Cartalax combinations with other bioregulators produce synergistic effects?
The relationship between the AED sequence and type XI collagen needs clarification. Understanding this structural similarity could improve peptide design for specific tissue targets.
Long-term effects on cellular function require more study. Most research examines short-term responses, but sustained epigenetic changes could produce different outcomes over time.
Tissue specificity mechanisms deserve attention. Why does this particular amino acid sequence target connective tissues while other bioregulators target different organs?
Potential In Vitro Research Applications
| Application Area | Research Focus | Cellular Models |
|---|---|---|
| Cellular Senescence Studies | p16/p21/p53 pathways, SIRT6 regulation, aging marker modulation | Primary fibroblasts, renal epithelial cells, aging cell cultures |
| Cartilage Biology | Chondrocyte proliferation, PCNA expression, matrix synthesis, ECM preservation | Chondrocyte cultures, cartilage explants, 3D tissue constructs |
| Extracellular Matrix Research | MMP-9 inhibition, collagen synthesis, matrix remodeling, structural protein expression | Fibroblast cultures, connective tissue models, matrix degradation assays |
| Gerontology Research | Age-related gene expression (IGF1, FOXO1, TERT), longevity pathways, cellular rejuvenation | Aged vs. young donor cells, senescent cell models, lifespan studies |
These applications represent active research areas where Cartalax offers unique experimental value. The peptide’s dual properties of epigenetic modulation and tissue specificity provide multiple angles for investigation.
Bottom Line
Cartalax provides researchers with a tool for studying tissue-specific bioregulation through direct DNA interaction. Its structural similarity to type XI collagen explains its selectivity for connective tissues.
The peptide’s effects on cellular aging markers prove particularly valuable. Reducing p16, p21, and p53 while increasing SIRT6 creates a molecular profile associated with cellular longevity.
Research demonstrates clear impacts on fibroblast function, cartilage regeneration, and kidney cell renewal. These findings support continued investigation into bioregulator mechanisms.
Laboratories studying cellular senescence, extracellular matrix biology, or age-related tissue changes may find Cartalax useful for their research protocols. The peptide’s well-characterized effects on specific molecular markers suit controlled experimental designs.
Cartalax is intended for research use only. Not intended for human consumption or any diagnostic or therapeutic use. Researchers should consult appropriate institutional guidelines and safety protocols when working with peptide compounds.
Scientific Reviewer
This research article has been scientifically reviewed and fact-checked by Dr. Ky H. Le, MD. Dr. Le earned his medical degree from St. George’s University School of Medicine and completed his residency training at Memorial Hermann Southwest Hospital. Board-certified in family medicine with experience in hospital medicine, he brings over two decades of clinical experience to reviewing research content and ensuring scientific accuracy.
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References
- V. Ashapkin, V. Khavinson, G. Shilovsky, N. Linkova, and B. Vanuyshin, “Gene expression in human mesenchymal stem cell aging cultures: modulation by short peptides,” Springer Science and Business Media LLC, May 2020. doi: 10.1007/s11033-020-05506-3. Available: https://doi.org/10.1007/s11033-020-05506-3
- M. Li et al., “p53 cooperates with SIRT6 to regulate cardiolipin de novo biosynthesis,” Springer Science and Business Media LLC, Sep. 2018. doi: 10.1038/s41419-018-0984-0. Available: https://doi.org/10.1038/s41419-018-0984-0
- V. Khavinson et al., “[Tripeptides slow down aging process in renal cell culture].,” Advances in gerontology = Uspekhi gerontologii, vol. 27 4, pp. 651–6, 2014.
- N. S. Lin’kova et al., “Peptide Regulation of Skin Fibroblast Functions during Their Aging In Vitro,” Springer Science and Business Media LLC, May 2016. doi: 10.1007/s10517-016-3370-x. Available: https://doi.org/10.1007/s10517-016-3370-x