BGPT: Create Graphs: Map phospho nodes in patient PBMCs

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Quick Analysis Plan Copied

The supplied evidence contains no patient PBMC phospho-node measurements—CIN85 phosphorylation data derive from HeLa/HuH7/SYF cell lines, and LDOC1 data from NSCLC cell lines and tumor tissue (). A PBMC phospho-node map therefore requires new phosphoproteomics input; only a cell-line-derived node map can be drafted from these records.

Long Analysis Plan

Evidence gap: no PBMC phospho data supplied

The only quantitative phospho-node values in the records come from cell-line experiments, not patient PBMCs. The CIN85 study reports: c-Cbl binding reduced ~80%, EGFR ubiquitination reduced ~70%, MVB sorting reduced >50% (p<0.0001), and EGFR degradation ~90% complete at 90 min in WT versus ~50% retained in the phospho-defective CIN85-4F mutant (). These nodes can seed a pathway graph, but they cannot substitute for PBMC measurements. To map phospho nodes in patient PBMCs you need raw phosphoproteomics (e.g., phospho-MS or phospho-flow) from PBMC samples—upload the patient data and the analysis can proceed with scanpy/anndata, kinase-substrate enrichment, and network mapping.

These are author-reported effect sizes from ≥30 cells/condition imaging assays and biochemical readouts in HeLa, HuH7, and SYF cells; overexpression and mutant-off-target effects are acknowledged limitations.

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Updated: September 17, 2026

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1. Src-mediated phosphorylation of CIN85 after EGF stimulation promotes CIN85 binding to the E3 ligase c-Cbl, enhancing EGFR ubiquitination and sorting into multivesicular bodies for degradation, whereas preventing CIN85 phosphorylation traps EGFR in early endosomes and delays degradation. [2012]

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2. LDOC1 interacts with clathrin adaptors AP1M1 and AP2M1 to regulate EGFR internalization and recycling, modulating EGFR signaling and gefitinib response in EGFR-mutant NSCLC, with LDOC1 loss promoting RTK activation and gefitinib resistance while associating with poorer patient outcomes. [2024]

9QualityResults Limitations Context Blindspots Methods Sample Conflict Data

↗ Paper Review ↗ Full Paper

3. This study demonstrates that pSTAT3 transactivates EGFR to maintain EGFR protein homeostasis and contributes to resistance against EGFR tyrosine kinase inhibitors in non-small cell lung cancer cells. [2024]

8QualityResults Limitations Context Blindspots Methods Sample Conflict

↗ Paper Review ↗ Full Paper

4. This study investigates the stereochemical consequences of phosphoenolpyruvate synthetase and pyruvate, orthophosphate dikinase on the P-Phospho and y-Phospho groups of ATP, revealing that the j3-phospho group retains configuration while the y-phospho group undergoes inversion during enzymatic reactions. [1985]

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↗ Paper Review ↗ Full Paper

5. This study investigates the relationship between EGFR gene copy number alterations and EGFR mutation status in lung adenocarcinoma, concluding that EGFR gene copy number as detected by SISH is not a reliable screening tool for selecting patients for EGFR mutation testing. [2014]

7QualityResults Limitations Context Blindspots Methods Sample Data

↗ Paper Review ↗ Full Paper

Key Insight

Phospho-node maps are only as good as their source tissue: EGFR-trafficking phospho-nodes measured in cancer cell lines may not even be expressed or phosphorylated in resting PBMCs, so transplanting cell-line nodes onto patient immune cells risks a false network.

Keep Exploring

Which phospho-nodes identified in EGFR-trafficking cell-line studies are detectably phosphorylated in resting versus stimulated human PBMCs?

What sample size and stimulation timepoints are needed to power a patient PBMC phospho-signaling network comparison?

Science Art

Science Movie

Make a narrated HD Science movie for this answer ($32 per minute)

Discussion

BGPT Bias

I default to flagging data-source mismatch (cell lines vs patient tissue) aggressively, which may read as obstructive when a proof-of-concept graph was intended.

Stay current without chasing every paper.

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Traceable Claims in Bioinformatics

See what computational analyses actually reported, with provenance for every claim.Know what the science actually supports before you trust the answer.

Explore by Goal

Quick Analysis Plan Copied

Long Analysis Plan

Evidence gap: no PBMC phospho data supplied

Top Data Sources Export MCP

1. Src-mediated phosphorylation of CIN85 after EGF stimulation promotes CIN85 binding to the E3 ligase c-Cbl, enhancing EGFR ubiquitination and sorting into multivesicular bodies for degradation, whereas preventing CIN85 phosphorylation traps EGFR in early endosomes and delays degradation. [2012]

2. LDOC1 interacts with clathrin adaptors AP1M1 and AP2M1 to regulate EGFR internalization and recycling, modulating EGFR signaling and gefitinib response in EGFR-mutant NSCLC, with LDOC1 loss promoting RTK activation and gefitinib resistance while associating with poorer patient outcomes. [2024]

3. This study demonstrates that pSTAT3 transactivates EGFR to maintain EGFR protein homeostasis and contributes to resistance against EGFR tyrosine kinase inhibitors in non-small cell lung cancer cells. [2024]

5. This study investigates the relationship between EGFR gene copy number alterations and EGFR mutation status in lung adenocarcinoma, concluding that EGFR gene copy number as detected by SISH is not a reliable screening tool for selecting patients for EGFR mutation testing. [2014]

Ask a Follow-Up

Key Insight

Phospho-node maps are only as good as their source tissue: EGFR-trafficking phospho-nodes measured in cancer cell lines may not even be expressed or phosphorylated in resting PBMCs, so transplanting cell-line nodes onto patient immune cells risks a false network.

Keep Exploring

Which phospho-nodes identified in EGFR-trafficking cell-line studies are detectably phosphorylated in resting versus stimulated human PBMCs?

What sample size and stimulation timepoints are needed to power a patient PBMC phospho-signaling network comparison?

Science Art

Science Movie

Make a narrated HD Science movie for this answer ($32 per minute)

Discussion

BGPT Bias

I default to flagging data-source mismatch (cell lines vs patient tissue) aggressively, which may read as obstructive when a proof-of-concept graph was intended.

Stay current without chasing every paper.

My BGPT

Trending

Traceable Claims in Bioinformatics

See what computational analyses actually reported, with provenance for every claim.Know what the science actually supports before you trust the answer.

Explore by Goal

Quick Analysis Plan Copied

Long Analysis Plan

Evidence gap: no PBMC phospho data supplied

Top Data Sources ExportMCP

1. Src-mediated phosphorylation of CIN85 after EGF stimulation promotes CIN85 binding to the E3 ligase c-Cbl, enhancing EGFR ubiquitination and sorting into multivesicular bodies for degradation, whereas preventing CIN85 phosphorylation traps EGFR in early endosomes and delays degradation. [2012]

2. LDOC1 interacts with clathrin adaptors AP1M1 and AP2M1 to regulate EGFR internalization and recycling, modulating EGFR signaling and gefitinib response in EGFR-mutant NSCLC, with LDOC1 loss promoting RTK activation and gefitinib resistance while associating with poorer patient outcomes. [2024]

3. This study demonstrates that pSTAT3 transactivates EGFR to maintain EGFR protein homeostasis and contributes to resistance against EGFR tyrosine kinase inhibitors in non-small cell lung cancer cells. [2024]

5. This study investigates the relationship between EGFR gene copy number alterations and EGFR mutation status in lung adenocarcinoma, concluding that EGFR gene copy number as detected by SISH is not a reliable screening tool for selecting patients for EGFR mutation testing. [2014]

Ask a Follow-Up

Key Insight

Phospho-node maps are only as good as their source tissue: EGFR-trafficking phospho-nodes measured in cancer cell lines may not even be expressed or phosphorylated in resting PBMCs, so transplanting cell-line nodes onto patient immune cells risks a false network.

Keep Exploring

Which phospho-nodes identified in EGFR-trafficking cell-line studies are detectably phosphorylated in resting versus stimulated human PBMCs?

What sample size and stimulation timepoints are needed to power a patient PBMC phospho-signaling network comparison?

Science Art

Science Movie

Make a narrated HD Science movie for this answer ($32 per minute)

Discussion

BGPT Bias

I default to flagging data-source mismatch (cell lines vs patient tissue) aggressively, which may read as obstructive when a proof-of-concept graph was intended.

Stay current without chasing every paper.

My BGPT

Trending

Top Data Sources Export MCP