**Figure 9.** Since activation of PKCs leads to their translocation to the particulate fraction, where they bind with their respective RACKs, we next measured RACK1 and RACK2 levels. RACK1 (58.53 ± 7.2, p < 0.05) and RACK2 (34.14 ± 8.2, p < 0.02) levels in the aging hippocampus were 41% and 66% lower than RACK1 and RACK2 levels in the young hippocampus, respectively (Figure 3a,b). RACK1 (121.95 ± 3.7, p < 0.02) and RACK2 (80.48 ± 11.5, p < 0.05) levels were also respectively 63% and 43% lower in the aging hippocampus compared to the middle-aged hippocampus (Figure 3a,b). RACK1 and RACK2 levels were not significantly different between the young and middle-age groups (Figure 3a,b), (Figure 4).

Description

Activated PKC translocation to membrane fractions is diminished in aged rats, with reduced binding to RACK scaffolding proteins contributing to impaired neuroprotective signaling.

More Figures from This Paper

$Subcellular distribution of PKC isoforms between cytosolic and membrane fractions is analyzed, showing altered translocation patterns in aged brain tissue.$

Figure 5

Subcellular distribution of PKC isoforms between cytosolic and membrane fractions is analyzed, showing altered translocation patterns in aged brain tissue.

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Figure 6

RACK1 and RACK2 scaffolding protein levels are measured in aging hippocampus, indicating reduced anchoring capacity for activated PKC isoforms.

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Figure 7

Western blot analysis of gamma, delta, and epsilon PKC levels in hippocampus across young, middle-aged, and aged rats demonstrates progressive age-related reduction.

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Figure 8

Quantitative densitometry of PKC isoform bands confirms statistically significant declines in neuroprotective PKC levels with advancing age.

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$Schematic representation of PKC isoform and RACK protein distribution in membrane fractions of young versus aged rat hippocampus illustrates the age-dependent loss of neuroprotective mechanisms.$

Figure 10

Schematic representation of PKC isoform and RACK protein distribution in membrane fractions of young versus aged rat hippocampus illustrates the age-dependent loss of neuroprotective mechanisms.

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Figure 11

RACK1 and RACK2 protein levels in hippocampal tissue are quantified by Western blot across three age groups, with both scaffolding proteins showing age-related reductions.

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Figure 9

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Source Paper

Age-Dependent Levels of Protein Kinase Cs in Brain: Reduction of Endogenous Mechanisms of Neuroprotection.

International journal of molecular sciences (2019)

PMID: 31331067

DOI: 10.3390/ijms20143544

Cite This Figure

![Figure 9: Activated PKC translocation to membrane fractions is diminished in aged rats, with reduced binding to RACK scaffolding proteins contributing to impaired neuroprotective signaling.](https://pdfs.citedhealth.com/figures/31331067/132.png)

> Source: Donatella Pastore et al. "Age-Dependent Levels of Protein Kinase Cs in Brain: Reduction of Endogenous Mech." *International journal of molecular sciences*, 2019. PMID: [31331067](https://pubmed.ncbi.nlm.nih.gov/31331067/)

<figure>
  <img src="https://pdfs.citedhealth.com/figures/31331067/132.png" alt="Activated PKC translocation to membrane fractions is diminished in aged rats, with reduced binding to RACK scaffolding proteins contributing to impaired neuroprotective signaling." />
  <figcaption>Figure 9. Activated PKC translocation to membrane fractions is diminished in aged rats, with reduced binding to RACK scaffolding proteins contributing to impaired neuroprotective signaling.<br>  Source: Donatella Pastore et al. "Age-Dependent Levels of Protein Kinase Cs in Brain: Reduction of Endogenous Mech." <em>International journal of molecular sciences</em>, 2019. PMID: <a href="https://pubmed.ncbi.nlm.nih.gov/31331067/">31331067</a></figcaption>
</figure>

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