Cellular Senescence and SASP Proteomics Service

Q: How does proteomics distinguish Senolytics from Senomorphics?

Senolytics (such as Navitoclax/ABT‑263 or Dasatinib + Quercetin) induce selective apoptosis in senescent cells by inhibiting anti‑apoptotic proteins (BCL‑2, BCL‑xL), leading to a reduction in total senescent biomass and the disappearance of all secretome output. In contrast, Senomorphics (such as Rapamycin or NF‑κB inhibitors) preserve senescent cell viability while selectively suppressing the transcription and secretion of pro‑inflammatory SASP factors (IL‑6, CXCL8, MMPs). Our paired intracellular and secretome DIA proteomics clearly differentiates these two mechanisms of action.

Q: What intracellular markers confirm true cellular senescence in the lysate?

Our whole‑cell DIA proteomics simultaneously quantifies key intracellular hallmarks: (1) upregulation of cyclin‑dependent kinase inhibitors p16 INK4a (CDKN2A) and p21 CIP1 (CDKN1A); (2) downregulation and loss of nuclear Lamin B1 (LMNB1); (3) depletion of nuclear HMGB1; (4) upregulation of pro‑survival BCL‑2 family proteins (BCL‑2, BCL‑xL, BCL‑W, MCL‑1); and (5) activation of senescence‑associated metabolic enzymes (GLS1 glutaminase).

Q: How does the SASP differ across replicative, oncogene‑induced, and therapy‑induced senescence?

While core factors like IL‑6, CXCL8, and IGFBP3 are common across multiple models, the broader SASP exhibits distinct trigger‑specific composition. Oncogene‑induced senescence (OIS, e.g., HRAS G12V ) produces an intense inflammatory signature dominated by CXCL1, CCL2, and IL‑1α. Therapy‑induced senescence (TIS, e.g., Doxorubicin or CDK4/6 inhibitors) is characterized by elevated extracellular matrix degradation enzymes (MMP3, MMP9) and high GDF15. Mitochondrial dysfunction (MiDAS) yields a distinct secretome lacking IL‑1α and IL‑6 but enriched in IL‑10 and TNF‑α. Our bioinformatic pipeline maps your experimental data directly against the reference SASP Atlas.

Q: Can you profile senescent cells and SASP in vivo from animal tissue samples?

Yes. For fresh‑frozen animal tissues (e.g., aging kidneys, fibrotic lungs, or irradiated tumors), we quantify tissue‑level senescence signatures (Lamin B1 loss, p16/p21 levels, extracellular matrix remodeling). If tissue cells are sorted by fluorescence‑activated cell sorting (FACS) using senescence reporter markers or C12FDG staining, our microscale 4D‑DIA workflow can quantify proteome remodeling from as few as 5 × 10⁴ sorted cells.

Q: What sample submission format and project metadata are required?

Samples should be submitted as flash‑frozen conditioned media supernatants (clarified at 2,000 × g) and/or matched flash‑frozen cell pellets (washed 2× with ice‑cold PBS). Please provide project metadata including: (1) cell type and species (human/mouse/rat), (2) senescence induction model (passage number, oncogene, compound concentration/duration), (3) control conditions (proliferating/untreated), (4) conditioning parameters (serum‑free duration, volume, cell count at harvest), and (5) requested analytical layers (secretome DIA, whole‑cell DIA, phosphoproteomics, EV‑SASP).

Unbiased SASP Secretome Profiling · Intracellular Senescence Biomarkers · Senolytic & Senomorphic MoA · 4D-DIA Proteomics

Cellular senescence is far more than a static cell-cycle arrest state; senescent cells remain metabolically hyperactive, secreting hundreds of pro-inflammatory cytokines, matrix metalloproteinases, and growth modulators collectively known as the Senescence-Associated Secretory Phenotype (SASP).

Creative Proteomics provides an integrated Cellular Senescence and SASP Proteomics Service designed to overcome the limitations of 20-plex antibody arrays. Combining strict serum-free conditioning protocols with high-depth DIA mass spectrometry, we simultaneously quantify intracellular senescence effectors (Lamin B1 loss, p16/p21, anti-apoptotic BCL-2 proteins) and resolve hundreds of soluble and extracellular vesicle SASP factors to advance longevity research and senotherapeutic drug discovery.

Dual intracellular & SASP secretome profiling: Quantifies cell-cycle arrest machinery alongside soluble cytokines, MMPs, and EV-associated factors
Inducer-specific SASP resolution: Maps distinct secretome profiles across replicative (RS), oncogene-induced (OIS), and therapy-induced senescence (TIS / CDK4/6i)
Senolytic vs. senomorphic drug deconvolution: Evaluates selective senescent cell elimination versus targeted paracrine SASP suppression
Albumin-free secretome workflow: Deploys 12–24 h defined serum-free conditioning pulses and 3 kDa ultrafiltration to eliminate bovine serum albumin (BSA) interference
Cell-size & biomass normalization: Corrects for the 2–4× hypertrophy of senescent cells, ensuring mathematically accurate per-cell secretome flux rates
SASP Atlas benchmarking: Direct bioinformatic mapping of experimental secretomes against reference human aging and senescence databases

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What Is Cellular Senescence and SASP Proteomics?

Definition & Core Capability: Cellular senescence and SASP proteomics is the high-resolution mass spectrometry-based identification and quantification of intracellular senescence effectors (such as p16^INK4a, p21^CIP1, Lamin B1 degradation, and anti-apoptotic BCL-2 proteins) and the comprehensive profiling of extracellular secreted bio-active molecules (SASP cytokines, chemokines, matrix metalloproteinases, shedding receptors, and extracellular vesicles). It bridges the gap between static cell-cycle arrest markers and dynamic, non-cell-autonomous paracrine tissue remodeling.

While senescent cells undergo permanent cell-cycle arrest via p53/p21^CIP1 (CDKN1A) and p16^INK4a (CDKN2A) tumor suppressor pathways, they remain metabolically hyperactive. Driven by persistent DNA damage response (DDR) signaling, cytoplasmic chromatin fragments (CCFs), and cGAS-STING/NF-κB activation, senescent cells secrete a complex, pro-inflammatory secretome termed the Senescence-Associated Secretory Phenotype (SASP).

Traditional assays—such as SA-β-gal staining or 20-plex Luminex/MSD bead arrays—capture only a narrow, pre-selected subset of inflammatory cytokines (e.g., IL-6, IL-8). However, unbiased proteomics studies (including the landmark SASP Atlas) prove that the genuine SASP comprises hundreds of distinct proteins that shift dynamically based on cell type, tissue microenvironment, and the initiating senescence stimulus. High-resolution DIA quantitative proteomics is the only unbiased methodology capable of simultaneously resolving intracellular senescence state markers and secretome flux rates.

Content Guide

SASP Multi-Layer Modules
Senescence Triggers & Models
Senolytic vs Senomorphic MoA
Serum-Free Conditioning SOP
Step-by-Step Workflow
Platform Decision Guide
Sample Submission Guidelines
Deliverables & Data Outputs

The Multi-Layer Architecture of the Senescent Cell Proteome

Our dual-layer proteomics approach captures both the intracellular arrest machinery and the multi-component extracellular secretome:

1. Intracellular Senescence Effectors

Direct quantification of cell-cycle arrest regulators (p16^INK4a, p21^CIP1), loss of nuclear lamina integrity (Lamin B1 / LMNB1 degradation), nuclear-to-cytoplasmic HMGB1 translocation, metabolic rewiring (GLS1 glutaminase), and pro-survival anti-apoptotic proteins (BCL-2, BCL-xL, BCL-W, MCL-1).

2. Soluble SASP Cytokines & Chemokines

Broad profiling of pro-inflammatory paracrine factors: IL-6, CXCL8 (IL-8), CCL2 (MCP-1), CXCL1, CXCL2, IL-1α (membrane-bound master regulator), and macrophage migration inhibitory factor (MIF) driving secondary bystander senescence and chronic tissue inflammation.

3. Matrix Metalloproteinases & ECM Regulators

Quantitative assessment of extracellular matrix remodeling enzymes (MMP1, MMP3, MMP9, MMP10, MMP12), collagen prolyl hydroxylases (P4HA1/2), and tissue inhibitors (TIMP1, TIMP2) promoting tissue fibrosis and pre-metastatic niche priming.

4. Growth Factors, Regulators & Shed Receptors

Comprehensive coverage of insulin-like growth factor binding proteins (IGFBP2, IGFBP3, IGFBP4, IGFBP7), growth differentiation factor 15 (GDF15), TGF-β1, shed receptor ectodomains (sTNF-R1/2, sIL-6R, sICAM-1, sEGFR), and extracellular vesicle (EV-SASP) tetraspanins (CD63, CD81).

Senescence Triggers, Biological Models, and Molecular Signatures

SASP expression profiles differ fundamentally across distinct senescence induction modalities:

Induction Trigger	Representative Model Systems	Core Signaling Pathway	Characteristic SASP & Proteomic Profile
Replicative Senescence (RS)	Primary human fibroblasts (WI-38, IMR-90), endothelial cells, MSCs (extended passage).	Telomere attrition, chronic DNA damage response (ATM/ATR → p53 → p21).	Lamin B1 loss, nuclear HMGB1 depletion, robust canonical SASP (IL-6, CXCL8, MMP1, IGFBP3/7).
Oncogene-Induced Senescence (OIS)	Primary cells expressing HRAS^G12V, BRAF^V600E, or PTEN loss.	Replication fork collapse, hyperactive MAPK signaling, p16^INK4a/RB tumor suppressor axis.	Hyper-inflammatory SASP: high CXCL1, CCL2, IL-1α, and elevated extracellular matrix proteases.
Therapy-Induced Senescence (TIS)	Cancer cell lines & stromal fibroblasts treated with Doxorubicin, Cisplatin, or Palbociclib.	CDK4/6 inhibition or double-strand DNA breaks, NF-κB and cGAS-STING activation.	High dependence on BCL-2/BCL-xL survival pathways, marked MMP3/9 secretion, elevated GDF15.
Mitochondrial Dysfunction (MiDAS)	Mitochondrial DNA depletion (rho-0), complex I/III inhibition, or POLG mutations.	AMPK activation, decreased NAD+/NADH ratio, p53 activation without IL-1α arm.	Distinct non-inflammatory SASP: elevated IL-10, IL-27, and TNF-α, with low IL-6 and IL-1α.
Paracrine / Bystander Senescence	Naïve cells cultured in senescent conditioned media or transwell co-cultures.	SASP receptor binding (IL-6R, CXCR2, TNFR) driving secondary ROS and DDR.	Secondary induction of p21, amplification of paracrine secretome, and loss of proliferative markers.

Senotherapeutic Drug Profiling: Senolytics vs. Senomorphics

Our platform quantitatively dissects the mechanism of action, potency, and selectivity of therapeutic candidates targeting senescence:

Senotherapy Class	Representative Compounds	Primary Mechanism of Action	Proteomic Evaluation Readout
Senolytics (Selective Elimination)	Navitoclax (ABT-263), ABT-737, Dasatinib + Quercetin (D+Q), Fisetin, UBX0101, CB-839 (GLS1i)	Inhibition of senescent cell anti-apoptotic pathways (SCAPs; BCL-2/BCL-xL/BCL-W), triggering selective apoptosis in senescent cells.	Selective reduction in senescent cell proteome biomass, induction of cleaved caspases, and global shutdown of secretome output.
Senomorphics (SASP Suppression)	Rapamycin (mTORi), Metformin, Ruxolitinib (JAKi), BIRB 796 (p38 MAPKi), QNZ (NF-κBi)	Inhibition of transcription factors (NF-κB, C/EBPβ) and translational pathways driving SASP production without killing senescent cells.	Selective downregulation of secreted cytokines, chemokines, and MMPs in conditioned media while maintaining cell viability.
Senoisolation & Tissue Profiling	Immuno-isolated or FACS-sorted senescent subsets from in vivo animal models (p16-reporter, C12FDG)	Evaluation of senolytic efficacy in complex, heterogeneous aging and fibrotic tissues.	Microscale 4D-DIA (dia-PASeF) quantifying proteome shifts from as few as 5×10⁴ sorted senescent cells from in vivo cohorts.

Pre-Analytical Protocol: Serum-Free Conditioning & Biomass Normalization

Bovine serum albumin (BSA) in standard culture media (~30–50 mg/mL) is 1,000× more abundant than endogenous secreted SASP factors (~10–100 μg/mL), completely suppressing mass spectrometry ionization. Furthermore, senescent cells exhibit significant cellular hypertrophy (2–4× larger protein biomass per cell). Creative Proteomics enforces a standardized secretome collection and mathematical normalization workflow:

Triple PBS Washing: Senescent monolayers and control cells are washed 3× with warm PBS to eliminate residual bovine serum proteins.
Defined Serum-Free Pulse (12–24 h): Cells are incubated in defined serum-free, phenol-red-free basal media for 12–24 hours (rigorously validated to maintain >95% cell viability without starvation stress).
Two-Step Centrifugation Clarification: Media is centrifuged at 300 × g (5 min) to remove floating cells, followed by 2,000 × g (10 min) to clear apoptotic debris.
3 kDa Ultrafiltration & Normalization: Supernatants are concentrated using 3 kDa MWCO ultrafiltration filters. Total protein is BCA-quantified and normalized to both viable cell counts (secretome output per 10⁶ cells) and intracellular protein biomass to eliminate hypertrophy bias.
Optional EV-SASP Fractionation: Differential ultracentrifugation (100,000 × g) or size-exclusion chromatography (SEC) separates soluble SASP proteins from exosomal / extracellular vesicle cargo (CD63, CD81).

Step-by-Step Cellular Senescence & SASP Proteomics Workflow

At Creative Proteomics, our senescence proteomics workflow ensures reproducible recovery, deep secretome coverage, and biological relevance at every phase.

Study Scoping & Induction Model Design

Define senescence triggers (RS, OIS, TIS, MiDAS), baseline proliferative controls, and senotherapeutic treatment arms (Senolytics vs. Senomorphics).

Serum-Free Conditioning & Harvest SOP

Execute 3× warm PBS washing and 12–24 h serum-free pulse. Harvest matched cell lysates and conditioned media supernatants in parallel.

Concentration, Digestion & EV Separation

Supernatants are concentrated via 3 kDa MWCO ultrafiltration. Automated S-Trap / SP3 processing delivers trypsin/Lys-C enzymatic digestion.

High-Resolution LC-MS/MS Acquisition

Single-shot DIA or 4D-DIA (dia-PASeF on timsTOF Pro 2) and Orbitrap Astral platforms with interleaved pooled QC injections.

Biomass Normalization & Contrast Modeling

Secretome protein intensities are normalized against viable cell counts or lysate protein biomass. Statistical contrasts apply limma FDR ≤ 0.05.

SASP Atlas Benchmarking & Reporting

Bioinformatic mapping against the reference SASP Atlas, GSEA pathway enrichment, KSEA kinase activity networks, and PRM validation shortlists.

Study Design

Trigger & control definition

Serum-Free Pulse

12–24 h conditioning SOP

Cleanup & Digest

3 kDa ultrafiltration & S-Trap

DIA / 4D-MS

timsTOF / Orbitrap with pooled QC

QC & Statistics

Biomass normalization & FDR ≤ 0.05

SASP Atlas Report

GSEA pathways & senolytic score

Albumin-free secretome workflow: strict 12–24 h conditioning eliminates BSA mass spec interference
Dual intracellular + secretome profiling: track cell-cycle arrest (LMNB1, p16/p21) alongside paracrine SASP flux
Cell hypertrophy correction: dual normalization by cell count and total biomass prevents quantification bias
Senotherapy mechanism deconvolution: clear differentiation of senolytics (clearance) vs. senomorphics (SASP blockade)
Direct SASP Atlas benchmarking: match experimental profiles against curated human aging biomarker databases

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Cellular Senescence & SASP Proteomics Analytical Platform Decision Guide

Match your senescence model, sample type, and biological question with the optimal acquisition strategy and mass spectrometry platform.

Study Objective & Scenario	Recommended Strategy	Primary MS Platform	Technical Rationale & Deliverables
Unbiased SASP Secretome Discovery (Conditioned Media / Fibroblasts / TIS Models)	Discovery DIA Secretome Proteomics	Orbitrap Astral / Exploris 480 / timsTOF Pro 2	Single-shot depth (>1,500–2,500+ secreted proteins), CV < 15%, deep coverage of low-abundance cytokines, MMPs, IGFBPs, and shed receptors.
Dual Intracellular Biomass & Secretome Coupling (Matched Cell Pellets + Conditioned Media)	Paired Whole-Cell & Secretome DIA Profiling	Orbitrap Exploris 480 / timsTOF Pro 2	Simultaneous quantification of >6,500+ intracellular proteins (LMNB1, p16/p21, BCL-2) and secretome output, correlating cellular state with paracrine flux.
Senolytic Clearance & Apoptotic Kinetics (Drug Screening / Navitoclax, D+Q Dose-Response)	High-Throughput 4D-DIA Proteomics	timsTOF Pro 2 (dia-PASeF)	Rapid short-gradient runs with high quantitative precision evaluating dose-dependent senescent cell depletion and SCAP pathway targeting.
Senescence Stress Kinase Activation (p38 MAPK, NF-κB, cGAS-STING, DDR Kinetics)	4D Phosphoproteomics (Ti-IMAC / Fe-NTA Enrichment)	timsTOF Pro 2 (TIMS-DIA) / Orbitrap Exploris 480	Captures >15,000–25,000+ phosphosites; Kinase-Substrate Enrichment Analysis (KSEA) maps upstream kinase networks regulating SASP transcription.
Targeted SASP Biomarker Validation Panels (Clinical Cohorts / Preclinical Plasma Testing)	Targeted PRM / 4D-PRM Panels	Orbitrap PRM / Triple Quadrupole (TSQ Altis / QTRAP 6500+)	Absolute or relative quantification of curated 30–60 SASP biomarker panels across longitudinal drug treatment cohorts with zero missing values.

Sample Submission Guidelines

Sample Category	Recommended Input	Minimum Feasibility	Harvesting & Shipping Guidelines
Conditioned Media (SASP Secretome)	2–5 mL conditioned medium per replicate	1 mL medium	Serum-free pulse (12–24 h); clarify at 2,000 × g (10 min); flash-freeze supernatant in cryovials. Ship on dry ice (-80°C).
Matched Senescent Cell Pellets	1–5 × 10⁶ cells (20–50 μg protein)	2 × 10⁵ cells (≥2 μg protein)	Wash 2× with cold PBS; aspirate completely; flash-freeze dry pellet in liquid N₂. Ship on dry ice.
Senescent Tissues / In Vivo Biopsies	20–50 mg wet weight	5 mg wet weight	Dissect rapidly; snap-freeze immediately in liquid N₂; avoid repeated freeze-thaw cycles. Ship on dry ice.
Extracellular Vesicles (EV-SASP)	10–20 mL conditioned medium or isolated EV pellet	5 mL medium	Condition in EV-depleted or serum-free medium; clarify; ship on dry ice.
Senescence Phosphoproteomics	5–10 × 10⁶ cells (100–200 μg protein)	50 μg total protein	Lyse in buffer with PhosSTOP and 1 mM sodium orthovanadate; flash-freeze. Ship on dry ice.

Deliverables and Decision-Ready Outputs

Quantitative secretome matrices, SASP Atlas benchmarking, and pathway scorecards

PCA clustering of proliferative, senescent, and senolytic-treated states

Sample-level PCA/UMAP evaluates global clustering across control, senescent, and senolytic/senomorphic treated cohorts.

Heatmap of SASP secretome factors across senescence triggers

Hierarchical clustering resolves distinct SASP modules (inflammatory cytokines, MMPs, IGFBPs) across induction models.

Volcano plot of senescent versus control differential secretome

Differential volcano plots prioritize statistically significant SASP factors, shed receptors, and anti-apoptotic proteins.

SASP Atlas pathway enrichment and stress kinase network

GSEA pathway enrichment and KSEA kinase networks map upstream drivers (NF-κB, p38 MAPK, cGAS-STING) controlling SASP flux.

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Normalized SASP & Lysate Data

Protein- and peptide-level normalized intensity matrices for both intracellular lysates and conditioned media secretomes.

Quality Assessment Summary

Sample-level QC, cell viability validation, digestion metrics, pooled QC CV distributions, and reproducibility reports.

SASP Atlas Benchmarking

Direct mapping of identified secretome factors against the reference SASP Atlas database for inducer-specific matching.

Pathway & Kinase Networks

GSEA functional pathway enrichment, KSEA kinase activity networks, and senolytic clearance scorecards.

Comprehensive Final Report

Publication-ready figures, auditable methods documentation, and candidate shortlists for targeted PRM validation.

Cellular Senescence & SASP Proteomics Frequently Asked Questions

How do you collect conditioned media without bovine serum albumin (BSA) contamination?

Bovine serum albumin (BSA) in standard culture media (~30–50 mg/mL) creates severe ionization suppression that masks low-abundance secreted cytokines (~10–100 μg/mL). We implement a strict 3-step washing procedure using warm PBS to remove serum residues, followed by incubation in defined serum-free, phenol-red-free basal media for 12–24 hours. Cell viability is verified to remain >95% to ensure the secretome reflects active paracrine secretion rather than non-specific apoptotic lysis.

How does proteomics distinguish Senolytics from Senomorphics?

Senolytics (such as Navitoclax/ABT-263 or Dasatinib + Quercetin) induce selective apoptosis in senescent cells by inhibiting anti-apoptotic proteins (BCL-2, BCL-xL), leading to a reduction in total senescent biomass and the disappearance of all secretome output. In contrast, Senomorphics (such as Rapamycin or NF-κB inhibitors) preserve senescent cell viability while selectively suppressing the transcription and secretion of pro-inflammatory SASP factors (IL-6, CXCL8, MMPs). Our paired intracellular and secretome DIA proteomics clearly differentiates these two mechanisms of action.

Can mass spectrometry profile both soluble SASP and extracellular vesicle (EV-SASP) cargo?

Yes. While soluble cytokines, chemokines, and MMPs are recovered in clarified conditioned media concentrated via 3 kDa ultrafiltration, extracellular vesicles (exosomes) can be fractionated using differential ultracentrifugation (100,000 × g) or size-exclusion chromatography (SEC). Our DIA platform can profile the soluble secretome and EV-associated proteome in parallel, identifying EV markers (CD63, CD81, TSG101) alongside vesicle-encapsulated signaling proteins.

What intracellular markers confirm true cellular senescence in the lysate?

Our whole-cell DIA proteomics simultaneously quantifies key intracellular hallmarks: (1) upregulation of cyclin-dependent kinase inhibitors p16^INK4a (CDKN2A) and p21^CIP1 (CDKN1A); (2) downregulation and loss of nuclear Lamin B1 (LMNB1); (3) depletion of nuclear HMGB1; (4) upregulation of pro-survival BCL-2 family proteins (BCL-2, BCL-xL, BCL-W, MCL-1); and (5) activation of senescence-associated metabolic enzymes (GLS1 glutaminase).

How does the SASP differ across replicative, oncogene-induced, and therapy-induced senescence?

While core factors like IL-6, CXCL8, and IGFBP3 are common across multiple models, the broader SASP exhibits distinct trigger-specific composition. Oncogene-induced senescence (OIS, e.g., HRAS^G12V) produces an intense inflammatory signature dominated by CXCL1, CCL2, and IL-1α. Therapy-induced senescence (TIS, e.g., Doxorubicin or CDK4/6 inhibitors) is characterized by elevated extracellular matrix degradation enzymes (MMP3, MMP9) and high GDF15. Mitochondrial dysfunction (MiDAS) yields a distinct secretome lacking IL-1α and IL-6 but enriched in IL-10 and TNF-α. Our bioinformatic pipeline maps your experimental data directly against the reference SASP Atlas.

What is the minimum volume of conditioned media required for SASP profiling?

For standard discovery DIA secretome proteomics, we recommend submitting 2–5 mL of conditioned medium per biological replicate (conditioned from 1–3 × 10⁶ cells). Following 3 kDa ultrafiltration concentration, this typically yields 10–50 μg of total secreted protein. For microscale or low-yield formats, robust profiling can be achieved from as little as 1 mL conditioned medium using high-sensitivity 4D-DIA (dia-PASeF).

Can you profile senescent cells and SASP in vivo from animal tissue samples?

Yes. For fresh-frozen animal tissues (e.g., aging kidneys, fibrotic lungs, or irradiated tumors), we quantify tissue-level senescence signatures (Lamin B1 loss, p16/p21 levels, extracellular matrix remodeling). If tissue cells are sorted by fluorescence-activated cell sorting (FACS) using senescence reporter markers or C12FDG staining, our microscale 4D-DIA workflow can quantify proteome remodeling from as few as 5 × 10⁴ sorted cells.

What sample submission format and project metadata are required?

Samples should be submitted as flash-frozen conditioned media supernatants (clarified at 2,000 × g) and/or matched flash-frozen cell pellets (washed 2× with ice-cold PBS). Please provide project metadata including: (1) cell type and species (human/mouse/rat), (2) senescence induction model (passage number, oncogene, compound concentration/duration), (3) control conditions (proliferating/untreated), (4) conditioning parameters (serum-free duration, volume, cell count at harvest), and (5) requested analytical layers (secretome DIA, whole-cell DIA, phosphoproteomics, EV-SASP).

* For Research Use Only. Not for use in the treatment or diagnosis of disease.

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