GO:0071363 cellular response to growth factor stimulus: Signaling Mechanism, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0071363 (cellular response to growth factor stimulus) describes any change in a cell's state or activity, such as movement, secretion, enzyme production, or gene expression, that occurs as a result of a growth factor stimulus.
• Growth factors such as PDGF-BB, IGF-1, NGF, and GAS6 activate receptor-mediated signaling that drives proliferation, migration, differentiation, and survival programs in target cells.
• The response is highly cell-type specific: for example, IGF-1 signaling mediates skeletal mechano-transduction in a cell-specific manner, and pericytes respond to PDGF-BB by secreting pro-regenerative molecules.
• Growth factor responses are dynamic and spatially organized, including the formation of flat clathrin lattices at the plasma membrane following growth factor stimulation.
• Dysregulated growth factor responses contribute to fibrosis, inflammation, angiogenesis, and cancer, making this GO term central to disease modeling.
• CRISPR knockout, point-mutation, knock-in, and overexpression models enable causal dissection of genes acting within GO:0071363, supported by CRISPR library screening and bioinformatics.
Description
The Gene Ontology term GO:0071363, cellular response to growth factor stimulus, is defined as any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a growth factor stimulus. Growth factors are extracellular polypeptides that bind cell-surface receptors and convert a transient ligand encounter into durable changes in cell behavior, including proliferation, migration, differentiation, survival, and secretory output. Because the same growth factor can elicit different outcomes in different cell types, the term captures a cell-intrinsic response rather than a fixed pathway. Mechanistically, growth factor binding initiates receptor activation and downstream signaling that can remodel the cytoskeleton, reprogram transcription, and alter the secretory repertoire of the cell. For example, platelet-derived growth factor-BB (PDGF-BB) stimulates pericytes to secrete pro-regenerative molecules, while insulin-like growth factor 1 (IGF-1) signaling mediates cell-specific skeletal mechano-transduction. Nerve growth factor (NGF) interacts with mast cells to modulate their behavior, and GAS6/PROS1 signaling on extracellular vesicles can attenuate inflammation. These examples illustrate that GO:0071363 encompasses ligand-specific, receptor-specific, and cell-type-specific responses. For researchers, GO:0071363 provides a unifying annotation framework for experiments that perturb growth factor signaling. It is relevant to angiogenesis, fibrosis, inflammation, and regenerative processes. Because the response is dynamic and spatially organized, including the formation of flat clathrin lattices after growth factor stimulation, it is best studied with a combination of genetic perturbation, imaging, and transcriptomic or proteomic readouts.
cellular response to growth factor stimulus At A Glance
| GO ID | GO:0071363 |
|---|---|
| GO term | cellular response to growth factor stimulus |
| Ontology | biological_process |
| Synonym | none |
| Definition | Any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a growth factor stimulus. |
| Major function | Transduces extracellular growth factor signals into changes in cell movement, secretion, enzyme production, and gene expression. |
| Example ligands | PDGF-BB, IGF-1, NGF, GAS6 |
| Example cell types | Pericytes, skeletal cells, mast cells, endothelial cells |
| Related processes | Angiogenesis, fibrosis, inflammation, mechano-transduction |
What Is GO:0071363?
In plain terms, GO:0071363 describes everything a cell does differently after it receives a growth factor signal. The official definition states that it is any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a growth factor stimulus. This includes rapid events such as cytoskeletal rearrangement and receptor internalization, as well as slower events such as changes in gene expression and secretory output. The term is a biological process annotation and is agnostic to the specific growth factor, receptor, or downstream pathway involved, so it can be applied across many cell types and experimental systems.
Why Is cellular response to growth factor stimulus Important in Cell Biology?
GO:0071363 is important because growth factor responses control fundamental cell decisions such as whether to proliferate, migrate, secrete, or survive, and because dysregulation of these responses underlies major human diseases including fibrosis, inflammation, and cancer. Studying this term helps researchers connect a specific ligand-receptor encounter to measurable cellular outputs, and it provides a standardized annotation for comparing results across cell types and experimental models.
• Growth factor responses drive cell movement, secretion, enzyme production, and gene expression changes that define tissue behavior.
• PDGF-BB stimulates pericytes to secrete pro-regenerative molecules, linking this term to tissue repair and regeneration.
• IGF-1 signaling mediates cell-specific skeletal mechano-transduction, connecting growth factor responses to mechanical cues in bone.
• NGF interactions with mast cells show that growth factor responses modulate immune cell behavior.
• GAS6/PROS1 and CD39/CD73 on extracellular vesicles attenuate inflammation, linking growth factor-related signaling to inflammatory control.
• TGF-beta/Smad signaling is a growth factor response pathway implicated in liver fibrosis and oxidative stress.
• Carbohydrate-recognition and angiogenesis studies connect growth factor responses to new blood vessel formation.
• Dynamic formation of flat clathrin lattices after growth factor stimulation shows that the response includes rapid membrane remodeling.
• Pericyte secretome studies highlight how growth factor responses shape the microenvironment through secreted factors.
• Because the response is cell-type specific, CRISPR models are needed to test causality gene by gene.
What Happens During cellular response to growth factor stimulus?
Growth factor recognition and receptor activation
In simple terms: A growth factor docks onto a receptor on the cell surface, like a key turning a lock.
The response begins when an extracellular growth factor engages its cognate cell-surface receptor. This ligand-receptor interaction is the defining trigger for GO:0071363. Examples include PDGF-BB acting on pericytes, IGF-1 acting in skeletal mechano-transduction, NGF interacting with mast cells, and GAS6/PROS1 signaling associated with extracellular vesicles. Receptor activation converts the extracellular cue into intracellular signals that initiate the cellular response.
Membrane remodeling and early signaling events
In simple terms: The cell surface reorganizes quickly, building platforms that help signals travel inward.
Following growth factor stimulation, the plasma membrane undergoes dynamic remodeling, including the formation of flat clathrin lattices. These early events are part of the cellular response and help organize signal transduction. The response is not a single linear step but a coordinated set of membrane and cytoskeletal changes that occur within minutes of stimulation.
Secretory reprogramming
In simple terms: The cell changes what it releases to influence its neighbors.
A major output of GO:0071363 is altered secretion. Pericytes secrete pro-regenerative molecules in response to PDGF-BB, and pericyte secretome composition is a key research focus. This secretory reprogramming allows the responding cell to modify its microenvironment and influence neighboring cells, linking growth factor responses to regeneration and tissue remodeling.
Gene expression and enzyme production changes
In simple terms: The cell switches genes on or off and changes the enzymes it makes.
The definition of GO:0071363 explicitly includes changes in gene expression and enzyme production. Growth factor signaling can activate transcription factors and alter the transcriptional program of the cell, leading to new protein synthesis and altered enzymatic activity. For example, TGF-beta/Smad signaling, a growth factor response pathway, is associated with changes in oxidative stress and inflammation-related gene expression in liver fibrosis models.
Cell movement and morphological change
In simple terms: The cell can move or change shape in response to the signal.
Cell movement is one of the state changes listed in the GO:0071363 definition. Growth factor responses can promote migration and morphological reorganization, which are relevant to angiogenesis and to mechano-transduction in skeletal cells. These motility changes depend on coordinated cytoskeletal and adhesion dynamics downstream of receptor activation.
Key Genes Involved in GO:0071363 cellular response to growth factor stimulus
The following genes and proteins are experimentally linked to growth factor responses and are commonly studied in the context of GO:0071363.
| Gene | Major Role | Research Relevance |
|---|---|---|
| PDGFB | Ligand that stimulates PDGF receptors | PDGF-BB induces pericyte secretion of pro-regenerative molecules |
| PDGFRB | Receptor for PDGF-BB | Mediates pericyte responses to PDGF-BB |
| IGF1 | Growth factor ligand | IGF-1 signaling mediates skeletal mechano-transduction |
| IGF1R | Receptor for IGF-1 | Transduces IGF-1 signals in mechano-responsive cells |
| NGF | Neurotrophic growth factor | Interacts with mast cells to modulate their behavior |
| GAS6 | Ligand associated with extracellular vesicles | GAS6/PROS1 on EVs attenuate inflammation |
| PROS1 | Ligand associated with extracellular vesicles | PROS1 with GAS6 on EVs attenuates inflammation |
| TGFB1 | Growth factor ligand | TGF-beta/Smad signaling in liver fibrosis and oxidative stress |
| SMAD2 | Intracellular signal transducer | Mediates TGF-beta signaling in fibrosis models |
| SMAD3 | Intracellular signal transducer | Mediates TGF-beta signaling in fibrosis models |
| CLTC | Clathrin heavy chain | Involved in flat clathrin lattice formation after growth factor stimulus |
| CLTB | Clathrin light chain | Component of clathrin lattices at the membrane |
| CD39 | Ectonucleotidase on extracellular vesicles | CD39/CD73 on EVs attenuate inflammation |
| CD73 | Ectonucleotidase on extracellular vesicles | CD39/CD73 on EVs attenuate inflammation |
| VEGFA | Angiogenic growth factor | Linked to angiogenesis and carbohydrate-recognition studies |
| KDR | VEGF receptor | Mediates angiogenic growth factor responses |
| ACTA2 | Pericyte/smooth muscle marker | Used to study pericyte responses and secretome |
| RGS5 | Pericyte marker | Used in pericyte biology and growth factor response studies |
How Is cellular response to growth factor stimulus Regulated?
The cellular response to growth factor stimulus is regulated at multiple levels. Ligand availability and receptor expression determine whether a cell can respond, as seen with PDGF-BB and pericytes and IGF-1 in skeletal mechano-transduction. Membrane dynamics, including the formation of flat clathrin lattices, regulate the spatial and temporal organization of the response. Downstream signaling nodes such as Smad proteins mediate transcriptional outputs of TGF-beta family growth factors. Secretory output is also regulated, as pericytes change their secretome in response to PDGF-BB. In addition, extracellular vesicle-associated ligands such as GAS6/PROS1 and ectoenzymes CD39/CD73 can modulate inflammatory signaling in the extracellular space. Together, these layers of regulation ensure that growth factor responses are context-dependent and cell-type specific.
cellular response to growth factor stimulus and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| TGFB1 | Liver fibrosis and oxidative stress | Knockout or point-mutation in hepatic cell lines; fibrosis induction models |
| SMAD2 | TGF-beta signaling in fibrosis | Knockout in liver cells followed by TGF-beta stimulation |
| SMAD3 | TGF-beta signaling in fibrosis | Knockout or knock-in reporter for Smad3 activity |
| GAS6 | Inflammation attenuation via EVs | Overexpression or knockout in EV-producing cells |
| PROS1 | Inflammation attenuation via EVs | Overexpression or knockout in EV-producing cells |
| PDGFB | Pericyte-mediated regeneration | Knockout or overexpression in pericyte cultures |
| IGF1 | Skeletal mechano-transduction | Knockout or point-mutation in bone-derived cells |
Growth factor responses in fibrosis
TGF-beta/Smad signaling is a growth factor response pathway implicated in liver fibrosis. In a mouse model, Aloin attenuated oxidative stress, inflammation, and CCl4-induced liver fibrosis, with a possible role of TGF-beta/Smad signaling. This links GO:0071363 to fibrotic disease mechanisms and suggests that modulating growth factor responses could be therapeutically relevant.
Growth factor responses in inflammation
Plasma extracellular vesicle surface-located GAS6/PROS1 and CD39/CD73 attenuate inflammation. Because GAS6 is a growth factor-related ligand, this connects GO:0071363 to inflammatory regulation and to extracellular vesicle biology. NGF interactions with mast cells further illustrate how growth factor responses modulate immune cell behavior.
Growth factor responses in angiogenesis and cancer
Carbohydrate-recognition and angiogenesis studies link growth factor responses to new blood vessel formation. Angiogenesis is a hallmark of tumor progression, and growth factors such as VEGF drive endothelial cell responses. This makes GO:0071363 relevant to cancer biology and to anti-angiogenic research.
Growth factor responses in tissue regeneration
Pericytes secrete pro-regenerative molecules in response to PDGF-BB, and pericyte secretome composition is studied in regenerative contexts. These findings connect GO:0071363 to tissue repair and regenerative medicine, where growth factor responses shape the local microenvironment.
From cellular response to growth factor stimulus-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is a candidate gene required for growth factor-induced secretion? | CRISPR knockout in pericyte-like cells followed by PDGF-BB stimulation |
| Does a specific phosphosite mediate growth factor signaling? | Point mutation knock-in of the phospho-acceptor residue |
| Can a reporter track growth factor-induced transcription? | Knock-in of a fluorescent reporter at a target locus |
| Does overexpression of a ligand enhance the response? | Overexpression of PDGFB or GAS6 in target cells |
| Which genes regulate membrane remodeling after stimulation? | CRISPR knockout library screening with imaging readout |
| Does a disease variant alter growth factor response? | Point-mutation knock-in of the variant followed by ligand stimulation |
How to Study the cellular response to growth factor stimulus Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Live-cell imaging | Membrane remodeling and clathrin lattice dynamics | Studying early events after growth factor stimulation |
| RNA-seq | Changes in gene expression | Identifying transcriptional outputs of growth factor signaling |
| Secretome proteomics | Secreted protein profile | Measuring secretory reprogramming in pericytes |
| Extracellular vesicle analysis | EV surface ligands and ectoenzymes | Studying inflammation modulation by GAS6/PROS1 and CD39/CD73 |
| Western blot | Phosphorylation of signaling proteins | Confirming pathway activation after ligand stimulation |
| Immunofluorescence | Protein localization and cell morphology | Visualizing pericyte or membrane responses |
| CRISPR library screening | Gene requirements for the response | Identifying regulators of growth factor-induced phenotypes |
| Bioinformatics pathway analysis | Enrichment of signaling pathways | Interpreting omics data in the context of GO:0071363 |
Imaging membrane dynamics
Live-cell imaging can capture the formation of flat clathrin lattices after growth factor stimulation. This method measures the spatial and temporal organization of the early response and is useful for studying membrane remodeling events within GO:0071363.
Transcriptomic profiling
RNA sequencing before and after growth factor stimulation measures changes in gene expression, which is one of the state changes included in the GO:0071363 definition. This approach can identify transcriptional programs downstream of TGF-beta/Smad signaling and other growth factor pathways.
Secretome analysis
Proteomic analysis of conditioned medium measures secretory reprogramming, a key output of GO:0071363. Pericyte secretome studies show that PDGF-BB changes the profile of secreted pro-regenerative molecules.
Extracellular vesicle characterization
Isolation and analysis of extracellular vesicles can detect surface ligands such as GAS6/PROS1 and ectoenzymes CD39/CD73 that modulate inflammation. This method connects growth factor responses to intercellular communication.
How CRISPR Can Be Used to Study GO:0071363 cellular response to growth factor stimulus
Knockout
CRISPR knockout is used to test whether a candidate gene is required for the cellular response to growth factor stimulus. For example, knocking out PDGFB or its receptor can determine whether pericyte secretion depends on PDGF-BB signaling. Knockout of TGFB1 or SMAD genes can test their role in fibrosis-related growth factor responses.
Point Mutation
Point mutation knock-in allows precise testing of specific residues, such as phosphorylation sites, in growth factor signaling proteins. This is valuable for dissecting IGF-1 signaling in skeletal mechano-transduction and for modeling disease-associated variants in TGF-beta pathway genes.
Knock-in
Knock-in of reporters or tags enables tracking of growth factor responses in live cells. For example, a fluorescent reporter knocked into a growth factor-responsive locus can measure transcriptional activation after stimulation. Tagged knock-in of clathrin components can help visualize membrane remodeling.
Overexpression
Overexpression of growth factors or their receptors can amplify the response and test sufficiency. Overexpressing PDGFB can enhance pericyte secretion, and overexpressing GAS6 or PROS1 can increase extracellular vesicle-mediated inflammation attenuation.
How EDITGENE Supports cellular response to growth factor stimulus Research
Researchers studying cellular response to growth factor stimulus-related genes often need to determine whether a candidate gene is causally involved in the response or merely correlated with it. CRISPR-based models provide the causal evidence needed to move from association to mechanism, and EDITGENE offers a full suite of services to generate and characterize these models.
Contact EDITGENE today to design your custom CRISPR model for cellular response to growth factor stimulus research.
Frequently Asked Questions About cellular response to growth factor stimulus
What is GO:0071363 cellular response to growth factor stimulus?
GO:0071363 is a Gene Ontology biological process term defined as any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a growth factor stimulus.
What genes are involved in cellular response to growth factor stimulus?
Genes and proteins experimentally linked to this term include PDGFB, PDGFRB, IGF1, IGF1R, NGF, GAS6, PROS1, TGFB1, SMAD2, SMAD3, CLTC, CLTB, CD39, CD73, VEGFA, and KDR.
How does PDGF-BB affect pericytes?
PDGF-BB stimulates pericytes to secrete pro-regenerative molecules, demonstrating a secretory response within GO:0071363.
What is the role of IGF-1 signaling in skeletal mechano-transduction?
IGF-1 signaling mediates cell-specific skeletal mechano-transduction, linking growth factor responses to mechanical cues in bone.
How does NGF interact with mast cells?
NGF interacts with mast cells and modulates their behavior, illustrating an immune cell growth factor response.
What is the connection between GAS6/PROS1 and inflammation?
Plasma extracellular vesicle surface-located GAS6/PROS1 and CD39/CD73 attenuate inflammation, linking growth factor-related signaling to inflammatory control.
What happens to the membrane after growth factor stimulation?
Growth factor stimulation can induce the dynamic formation of flat clathrin lattices at the plasma membrane.
How is TGF-beta/Smad signaling related to liver fibrosis?
TGF-beta/Smad signaling is a growth factor response pathway implicated in CCl4-induced liver fibrosis, oxidative stress, and inflammation in mice.
What research methods are used to study GO:0071363?
Common methods include live-cell imaging of membrane dynamics, RNA-seq for gene expression changes, secretome proteomics, extracellular vesicle analysis, and CRISPR library screening.
How can CRISPR models help study cellular response to growth factor stimulus?
CRISPR knockout, point mutation, knock-in, and overexpression models allow causal testing of specific genes and residues in growth factor responses, such as PDGFB in pericytes or SMAD genes in fibrosis.
Conclusion
GO:0071363 cellular response to growth factor stimulus is a broad but experimentally tractable biological process that connects extracellular growth factor signals to changes in cell movement, secretion, enzyme production, and gene expression. Its relevance spans regeneration, fibrosis, inflammation, and angiogenesis, with key roles for ligands such as PDGF-BB, IGF-1, NGF, GAS6, and TGF-beta. Because the response is cell-type specific and dynamically regulated, CRISPR-based causal models are essential for dissecting the underlying mechanisms. EDITGENE provides knockout, point-mutation, knock-in, overexpression, library screening, and bioinformatics services to support research on this important Gene Ontology term.
References
- 1. Gaceb A et al.. 2018. Pericyte Secretome.. Adv Exp Med Biol 1109:139-163 PMID: 30523595
- 2. Bai J et al.. 2023. Aloin Attenuates Oxidative Stress, Inflammation, and CCl(4)-Induced Liver Fibrosis in Mice: Possible Role of TGF-β/Smad Signaling.. J Agric Food Chem 71(49):19475-19487 PMID: 38038700
- 3. Fabiano MP et al.. 2025. Plasma extracellular vesicle surface-located GAS6/PROS1 and CD39/CD73 attenuate inflammation.. Cell Rep 44(8):116096 PMID: 40751911
- 4. Nangia-Makker P et al.. 2000. Carbohydrate-recognition and angiogenesis.. Cancer Metastasis Rev 19(1-2):51-7 PMID: 11191063
- 5. Tian F et al.. 2018. IGF-1 signaling mediated cell-specific skeletal mechano-transduction.. J Orthop Res 36(2):576-583 PMID: 28980721
- 6. Gaceb A et al.. 2018. Pericytes secrete pro-regenerative molecules in response to platelet-derived growth factor-BB.. J Cereb Blood Flow Metab 38(1):45-57 PMID: 28741407
- 7. Kritas SK et al.. 2014. Nerve growth factor interactions with mast cells.. Int J Immunopathol Pharmacol 27(1):15-9 PMID: 24674674
- 8. Qiao L et al.. 2026. Dynamics of the formation of flat clathrin lattices in response to growth factor stimulus.. PLoS Comput Biol 22(3):e1014013 PMID: 41811876
