# Cell Press Summary, Highlights, and eTOC Examples

Examples of Cell Press-specific elements including Summary (abstract), Highlights, and eTOC blurb.

---

## Complete Example 1: Senescence and Aging

### Summary (150 words max)

```
Cellular senescence is a stress response that prevents damaged cell 
proliferation but can drive tissue dysfunction through the senescence-
associated secretory phenotype (SASP). How senescent cells resist 
apoptosis despite expressing pro-apoptotic p53 has remained unclear. 
Here, we identify FOXO4 as a pivotal mediator of senescent cell viability. 
FOXO4 is highly expressed in senescent cells and directly interacts with 
p53, retaining it in the nucleus and preventing p53-mediated apoptosis. 
A cell-permeable peptide that disrupts FOXO4-p53 interaction selectively 
induces p53 nuclear exclusion and apoptosis in senescent cells without 
affecting proliferating cells. In vivo, this FOXO4 peptide neutralizes 
doxorubicin-induced senescent cells and restores fitness, fur density, 
and renal function in naturally aged mice. These findings establish 
FOXO4-mediated p53 sequestration as a senescence-specific survival 
pathway and demonstrate the therapeutic potential of targeted senescent 
cell elimination.
```

### Highlights (≤85 characters each)

```
• FOXO4 is selectively upregulated in senescent cells and binds p53

• FOXO4-p53 interaction retains p53 in the nucleus, preventing apoptosis

• A FOXO4-targeting peptide induces apoptosis specifically in senescent cells

• FOXO4 peptide treatment restores fitness and organ function in aged mice
```

### eTOC Blurb (30-50 words)

```
Baar et al. identify FOXO4 as a critical mediator of senescent cell survival 
through p53 sequestration. A peptide disrupting FOXO4-p53 interaction 
selectively eliminates senescent cells and restores tissue function in 
aged mice, establishing proof-of-concept for targeted senolytic therapy.
```

### In Brief (1 sentence)

```
A FOXO4-targeting peptide selectively eliminates senescent cells by 
releasing p53, restoring tissue function in aged mice.
```

---

## Complete Example 2: Genome Organization

### Summary (150 words max)

```
The three-dimensional organization of chromosomes within the nucleus 
influences gene expression, DNA replication, and genome stability. 
Phase separation has emerged as a potential mechanism for organizing 
nuclear contents, but whether condensates can shape chromosome 
structure in vivo remains unknown. Here, we show that the transcriptional 
coactivator BRD4 forms liquid-like condensates at super-enhancers that 
organize associated chromatin into hub structures. Optogenetic induction 
of BRD4 condensates is sufficient to remodel chromosome topology and 
activate transcription within minutes. Conversely, disruption of BRD4 
condensates with the small molecule JQ1 dissolves chromatin hubs and 
rapidly silences super-enhancer-controlled genes. Single-molecule 
tracking reveals that condensate formation increases the local 
concentration of transcription machinery 100-fold, explaining the 
transcriptional potency of super-enhancers. These results establish 
phase separation as a mechanism for chromatin organization and 
transcriptional control with implications for understanding and 
targeting oncogenic super-enhancers.
```

### Highlights

```
• BRD4 forms liquid condensates at super-enhancers in living cells

• BRD4 condensates organize chromatin into transcriptionally active hubs

• Optogenetic condensate induction rapidly remodels chromatin topology

• Condensates concentrate transcription machinery 100-fold locally
```

### eTOC Blurb

```
Sabari et al. demonstrate that BRD4 forms phase-separated condensates 
at super-enhancers that organize chromatin into hub structures and 
concentrate transcription machinery. Optogenetic manipulation reveals 
that condensate formation directly drives chromatin remodeling and 
transcriptional activation.
```

---

## Complete Example 3: Metabolism and Immunity

### Summary (150 words max)

```
Immune cells undergo dramatic metabolic reprogramming upon activation, 
switching from oxidative phosphorylation to aerobic glycolysis. This 
metabolic shift is thought to support the biosynthetic demands of 
rapid proliferation, but whether specific metabolites directly regulate 
immune cell function remains largely unexplored. Here, we show that 
the glycolytic metabolite phosphoenolpyruvate (PEP) sustains T cell 
receptor signaling by inhibiting sarco/endoplasmic reticulum Ca²⁺-ATPase 
(SERCA) activity. PEP accumulates in activated T cells and directly 
binds SERCA, preventing calcium reuptake and prolonging store-operated 
calcium entry. Genetic or pharmacological enhancement of PEP levels 
augments T cell effector function and anti-tumor immunity in vivo. 
Conversely, tumor-derived lactate suppresses PEP levels and impairs 
T cell calcium signaling, contributing to tumor immune evasion. These 
findings reveal an unexpected signaling role for a glycolytic 
intermediate and suggest metabolic strategies to enhance T cell 
responses in cancer immunotherapy.
```

### Highlights

```
• Phosphoenolpyruvate (PEP) accumulates during T cell activation

• PEP directly binds and inhibits SERCA to sustain calcium signaling

• Enhancing PEP levels augments anti-tumor T cell immunity

• Tumor lactate suppresses T cell PEP levels and calcium signaling
```

### eTOC Blurb

```
Ho et al. discover that the glycolytic metabolite phosphoenolpyruvate 
directly regulates T cell calcium signaling by inhibiting SERCA. This 
metabolic-signaling link is exploited by tumors through lactate 
secretion and offers new targets for cancer immunotherapy.
```

---

## Graphical Abstract Description Examples

### For Senescence Paper

```
"Graphical abstract for Cell paper on FOXO4 and senescence:

Left panel: Senescent cell (enlarged, irregular shape) with FOXO4 (blue 
oval) binding p53 (green oval) in nucleus, preventing apoptosis. Label: 
'FOXO4 sequesters p53 → Senescent cell survival'

Center panel: Same senescent cell with FOXO4 peptide (red wedge) 
disrupting FOXO4-p53 interaction. p53 moves to mitochondria (orange 
organelles). Label: 'FOXO4 peptide disrupts interaction'

Right panel: Senescent cell undergoing apoptosis (fragmenting). Label: 
'Selective senescent cell death'

Bottom: Aged mouse (grey, hunched) → Treatment arrow → Rejuvenated mouse 
(brown, active). Label: 'Restored fitness in aged mice'

Color scheme: Blue for FOXO4, green for p53, red for peptide, grey 
background for cells."
```

### For Chromatin Paper

```
"Graphical abstract for Cell paper on BRD4 condensates:

Top row: Diagram showing BRD4 molecules (purple dots) clustering at 
super-enhancer (yellow region on DNA strand), forming condensate 
(purple droplet). Transcription factors (orange, green, blue small 
circles) accumulate inside condensate.

Middle: Chromatin fibers (grey) being pulled into hub structure around 
condensate. Arrow showing '100× local concentration increase'

Bottom: Two panels - Left shows 'JQ1' treatment dissolving condensate 
and chromatin hub dispersing. Right shows 'Optogenetic activation' 
creating new condensate with chromatin reorganization. Gene expression 
indicators (up arrow, down arrow) for each condition."
```

---

## Writing Tips for Cell Elements

### Summary Tips

1. **First sentence**: Establish the biological context
2. **Second sentence**: State what was unknown (the gap)
3. **"Here, we show/identify/demonstrate"**: Clear transition to your work
4. **Middle sentences**: Key findings with mechanism
5. **Final sentence**: Significance and implications

### Highlights Tips

- **Start with a noun or verb**: "FOXO4 forms..." or "Activation of..."
- **One finding per bullet**: Don't combine multiple points
- **Be specific**: Include the protein/gene/pathway name
- **Check character count**: Strictly ≤85 characters including spaces
- **Cover different findings**: Don't repeat the same point

### eTOC Blurb Tips

- **Start with author names**: "Smith et al. show that..."
- **One or two sentences only**: Keep it punchy
- **Include the key mechanism**: Not just the finding
- **End with significance**: Why readers should care

---

## Character Counting for Highlights

Use this to check your highlights:

```
• This highlight is exactly 52 characters long including sp
  ↑ Count: 52 characters ✓ (under 85)

• This highlight is getting close to the maximum allowed character limit
  ↑ Count: 73 characters ✓ (under 85)

• This highlight demonstrates what happens when you try to include way too much info
  ↑ Count: 88 characters ✗ (over 85 - need to shorten)
```

---

## See Also

- `cell_press_style.md` - Comprehensive Cell Press writing guide
- `nature_abstract_examples.md` - Compare with Nature abstract style

