GO:0097208 alveolar lamellar body: Components, Assembly and Research Methods, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0097208 alveolar lamellar body is a specialized secretory organelle found in type II pneumocytes that synthesizes, secretes, and reutilizes pulmonary surfactant.
• Lamellar body biogenesis depends on autophagy-related membrane trafficking and is regulated by GCN5L1 in mouse alveolar epithelial cells [1,2].
• Surfactant protein B (SFTPB) is trafficked to the lamellar body after synthesis, and Rab3D and actin define distinct lamellar body subpopulations [5,8].
• Lamellar body membrane turnover is stimulated by secretagogues, linking the organelle to regulated exocytosis.
• Ozone-induced alveolar injury causes sequential changes in lamellar body hydrolases and lamellar body responses during repair [3,6].
• CRISPR knockout, point-mutation, knock-in, and overexpression models in type II pneumocyte lines enable causal testing of lamellar body genes [1,2,5].
Description
The alveolar lamellar body (GO:0097208) is a specialized secretory organelle found in type II pneumocytes and is involved in the synthesis, secretion, and reutilization of pulmonary surfactant. Pulmonary surfactant is essential for reducing alveolar surface tension and maintaining alveolar stability, and the lamellar body is the principal intracellular storage compartment for surfactant lipids and proteins before secretion. Because surfactant homeostasis is critical for lung function, the lamellar body has become a focal point for researchers studying alveolar epithelial cell biology, surfactant metabolism, and lung injury repair [3,6]. At the cellular level, the lamellar body is not a static storage granule; its biogenesis, membrane turnover, and cargo trafficking are dynamically regulated [1,2,7]. Autophagy contributes to lamellar body formation and surfactant production in type 2 alveolar epithelial cells, and GCN5L1 modulates lamellar body biogenesis and trafficking in mouse alveolar epithelial cells [1,2]. Newly synthesized surfactant protein B is trafficked to the lamellar body, and Rab3D and actin reveal distinct lamellar body subpopulations in alveolar epithelial type II cells [5,8]. These findings establish the lamellar body as a membrane-trafficking hub whose dysfunction can impair surfactant production and lung repair [1,2,5]. For researchers, GO:0097208 provides a precise ontology anchor for annotating genes, proteins, and pathways that control surfactant storage and secretion. Experimental models of alveolar injury and repair, including ozone exposure in rats, have revealed sequential changes in lamellar body hydrolases and lamellar body responses, making the organelle a useful readout for epithelial injury and regeneration [3,6]. Understanding the molecular machinery that builds and maintains the lamellar body is therefore central to lung physiology and to developing targeted interventions for surfactant-related disorders [1,2,7].
alveolar lamellar body At A Glance
| GO ID | GO:0097208 |
|---|---|
| GO term | alveolar lamellar body |
| Ontology | cellular_component |
| Synonym | none |
| Definition | A specialized secretory organelle found in type II pneumocytes and involved in the synthesis, secretion, and reutilization of pulmonary surfactant. |
| Major function | Synthesis, storage, secretion, and reutilization of pulmonary surfactant. |
| Cell type | Type II pneumocytes (alveolar epithelial type II cells) [5,8]. |
| Key cargo | Surfactant proteins and lipids, including surfactant protein B (SFTPB). |
| Regulatory example | GCN5L1 regulates lamellar body biogenesis and trafficking in mouse alveolar epithelial cells. |
| Trafficking markers | Rab3D and actin define distinct lamellar body subpopulations. |
What Is GO:0097208?
The alveolar lamellar body (GO:0097208) is defined as a specialized secretory organelle found in type II pneumocytes and involved in the synthesis, secretion, and reutilization of pulmonary surfactant. In practical terms, it is a membrane-bound, lamellated storage compartment in alveolar type II cells where surfactant components are assembled, stored, and later released into the alveolar space [4,5].
Why Is alveolar lamellar body Important in Cell Biology?
The alveolar lamellar body is important because it is the central organelle for pulmonary surfactant storage and secretion, and surfactant is required for normal alveolar function. Disruption of lamellar body biogenesis or trafficking can impair surfactant production, and autophagy-dependent mechanisms contribute to lamellar body formation and surfactant production in type 2 alveolar epithelial cells [1,2]. Lamellar body membrane turnover is stimulated by secretagogues, indicating that the organelle is a regulated secretory compartment responsive to physiological signals. In injury models, ozone exposure causes sequential changes in lamellar body hydrolases and lamellar body responses during alveolar injury and repair, linking the organelle to epithelial stress and regeneration [3,6]. Consequently, GO:0097208 is a valuable ontology term for annotating genes and pathways in lung biology and for interpreting experimental models of surfactant dysfunction [1,2,5].
Core Ontology of GO:0097208 alveolar lamellar body
• Provides the intracellular storage site for pulmonary surfactant, which is essential for alveolar stability.
• Its biogenesis is regulated by GCN5L1 in mouse alveolar epithelial cells, linking metabolism to organelle formation.
• Autophagy contributes to lamellar body formation and surfactant production in type 2 alveolar epithelial cells.
• Surfactant protein B is trafficked to the lamellar body, making the organelle a key node in surfactant protein routing.
• Rab3D and actin define distinct lamellar body subpopulations, revealing heterogeneity in secretory granule organization.
• Lamellar body membrane turnover is stimulated by secretagogues, connecting the organelle to regulated exocytosis.
• Ozone-induced alveolar injury causes sequential changes in lamellar body hydrolases during injury and repair.
• Ozone-induced lamellar body responses in a rat model provide a tractable system for studying alveolar repair.
• The organelle is a cellular_component annotation target for genes involved in surfactant metabolism and lung disease.
• Lamellar body biology informs research on respiratory distress, alveolar injury, and epithelial regeneration [1,2,6].
What Happens During alveolar lamellar body?
(未命名小节)
In simple terms: The lamellar body is built, filled with surfactant, and then releases its contents when the cell receives the right signal.
The alveolar lamellar body is a specialized secretory organelle found in type II pneumocytes and is involved in the synthesis, secretion, and reutilization of pulmonary surfactant. Its life cycle includes biogenesis, cargo loading, storage, and regulated secretion. GCN5L1 regulates pulmonary surfactant production by modulating lamellar body biogenesis and trafficking in mouse alveolar epithelial cells, indicating that the formation and movement of the organelle are actively controlled. Autophagy also contributes to lamellar body formation and surfactant production in type 2 alveolar epithelial cells, linking degradative membrane pathways to organelle assembly. Newly synthesized surfactant protein B is trafficked to the lamellar body, showing that cargo delivery is a defined step in the organelle's maturation. Finally, lamellar body membrane turnover is stimulated by secretagogues, demonstrating that secretion and membrane recycling are regulated events.
Biogenesis and Autophagy Contribution
In simple terms: The cell uses autophagy-related machinery to help build the lamellar body.
Autophagy plays a role in lamellar body formation and surfactant production in type 2 alveolar epithelial cells. This indicates that membrane remodeling and degradative pathways are coupled to the generation of the lamellar body. In addition, GCN5L1 regulates lamellar body biogenesis and trafficking in mouse alveolar epithelial cells, providing a genetic handle on the biogenesis step. Together, these findings support a model in which the lamellar body arises through coordinated membrane trafficking and autophagy-related processes rather than as a simple budding event [1,2].
Cargo Trafficking to the Lamellar Body
In simple terms: Newly made surfactant proteins are packaged and sent to the lamellar body.
Trafficking of newly synthesized surfactant protein B to the lamellar body in alveolar type II cells has been demonstrated, establishing the lamellar body as a destination for surfactant protein cargo. Rab3D and actin reveal distinct lamellar body subpopulations in alveolar epithelial type II cells, suggesting that the organelle is heterogeneous and that cytoskeletal and small GTPase machinery participates in its organization. These observations indicate that cargo delivery and organelle identity are spatially and mechanistically distinct within type II pneumocytes [5,8].
Secretion and Membrane Turnover
In simple terms: When stimulated, the lamellar body releases surfactant and recycles its membrane.
Lamellar body membrane turnover is stimulated by secretagogues, showing that the organelle undergoes regulated exocytosis and membrane recycling in response to physiological cues. This secretory behavior is consistent with the definition of the alveolar lamellar body as a specialized secretory organelle involved in the secretion and reutilization of pulmonary surfactant. The coupling of secretion to membrane turnover implies that the lamellar body membrane is a dynamic compartment rather than a static shell.
Injury and Repair Responses
In simple terms: When the lung is injured, the lamellar body changes in measurable ways during damage and recovery.
Ozone-induced lamellar body responses in a rat model for alveolar injury and repair demonstrate that the organelle reacts to epithelial injury. Sequential changes of lamellar body hydrolases during ozone-induced alveolar injury and repair further show that enzymatic contents of the organelle are remodeled over the course of injury and recovery. These studies establish the lamellar body as a readout of alveolar epithelial stress and regeneration [3,6].
Key Genes Involved in GO:0097208 alveolar lamellar body
The following genes and proteins have been experimentally linked to alveolar lamellar body biology, including biogenesis, trafficking, secretion, and injury responses [1,2,3,5,6,7,8].
| Gene | Major Role | Research Relevance |
|---|---|---|
| GCN5L1 | Regulates pulmonary surfactant production by modulating lamellar body biogenesis and trafficking | Genetic handle for lamellar body biogenesis in mouse alveolar epithelial cells |
| Autophagy-related genes (general) | Contribute to lamellar body formation and surfactant production | Pathway-level target for autophagy-dependent organelle assembly |
| SFTPB | Newly synthesized surfactant protein B is trafficked to the lamellar body | Cargo marker for lamellar body trafficking studies |
| RAB3D | Defines distinct lamellar body subpopulations with actin | Small GTPase marker for lamellar body heterogeneity |
| Actin (ACTB/ACTG1) | Reveals distinct lamellar body subpopulations with Rab3D | Cytoskeletal component in lamellar body organization |
| Lamellar body hydrolases (general) | Sequential changes during ozone-induced alveolar injury and repair | Enzymatic readout of injury and repair |
| Surfactant lipid synthesis enzymes (general) | Involved in synthesis of pulmonary surfactant stored in lamellar bodies | Pathway context for surfactant metabolism |
| Surfactant protein processing enzymes (general) | Participate in surfactant protein maturation for lamellar body storage | Candidate genes for trafficking and processing studies |
| Secretagogue-responsive machinery (general) | Lamellar body membrane turnover is stimulated by secretagogues | Functional assay for regulated secretion |
| Alveolar type II cell markers (general) | Define the cell type in which lamellar bodies are found [5,8] | Cell identity context for organelle studies [5,8] |
| Ozone-responsive stress genes (general) | Associated with lamellar body responses during alveolar injury | Model system for injury and repair |
| Membrane trafficking regulators (general) | Modulate lamellar body biogenesis and trafficking | Broad class of candidate regulators |
| Autophagy machinery (general) | Supports lamellar body formation and surfactant production | Pathway for functional perturbation |
| Surfactant protein B trafficking machinery (general) | Directs SFTPB to the lamellar body | Trafficking route to dissect |
| Rab GTPase effectors (general) | Potential mediators of Rab3D-defined lamellar body subpopulations | Candidate interaction partners |
| Hydrolase enzymes (general) | Change sequentially during alveolar injury and repair | Biomarker candidates for injury models |
How Is alveolar lamellar body Regulated?
Lamellar body biology is regulated at multiple levels. GCN5L1 regulates pulmonary surfactant production by modulating lamellar body biogenesis and trafficking in mouse alveolar epithelial cells, indicating genetic control over organelle formation and movement. Autophagy contributes to lamellar body formation and surfactant production in type 2 alveolar epithelial cells, linking nutrient and membrane stress pathways to organelle assembly. Lamellar body membrane turnover is stimulated by secretagogues, showing that secretion and membrane recycling are under physiological regulation. In injury settings, ozone exposure induces sequential changes in lamellar body hydrolases and lamellar body responses, indicating that the organelle is remodeled during alveolar injury and repair [3,6]. Rab3D and actin further suggest that cytoskeletal and small GTPase-dependent mechanisms regulate lamellar body subpopulations.
alveolar lamellar body and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| GCN5L1 | Surfactant production and lamellar body biogenesis | Knockout or overexpression in mouse alveolar epithelial cells |
| Autophagy-related genes | Lamellar body formation and surfactant production | Autophagy perturbation in type 2 alveolar epithelial cells |
| SFTPB | Surfactant protein B trafficking to lamellar body | Tagged knock-in for trafficking imaging |
| RAB3D | Lamellar body subpopulation organization | Knockout or point mutation in alveolar epithelial type II cells |
| Lamellar body hydrolases | Alveolar injury and repair responses | Ozone-induced injury model with hydrolase profiling |
Surfactant Deficiency and Alveolar Instability
The alveolar lamellar body is involved in the synthesis, secretion, and reutilization of pulmonary surfactant, and surfactant is required for normal alveolar function. When lamellar body biogenesis or trafficking is impaired, surfactant production can be reduced, as shown by GCN5L1-dependent regulation of pulmonary surfactant production in mouse alveolar epithelial cells. Autophagy-dependent lamellar body formation and surfactant production further link organelle biology to surfactant availability in type 2 alveolar epithelial cells. These mechanisms are relevant to conditions characterized by surfactant deficiency and alveolar instability [1,2,4].
Alveolar Injury and Repair
Ozone-induced alveolar injury and repair models demonstrate that lamellar bodies respond dynamically to epithelial damage. Sequential changes of lamellar body hydrolases during ozone-induced alveolar injury and repair indicate that the organelle's enzymatic content is remodeled during both injury and recovery phases. These findings support the use of lamellar body parameters as readouts of alveolar epithelial stress and regeneration [3,6].
Secretory and Trafficking Dysfunction
Lamellar body membrane turnover is stimulated by secretagogues, and newly synthesized surfactant protein B is trafficked to the lamellar body, highlighting the importance of regulated secretion and cargo delivery [5,7]. Rab3D and actin reveal distinct lamellar body subpopulations, suggesting that defects in cytoskeletal or small GTPase-dependent organization could alter organelle heterogeneity and function. Such trafficking defects are conceptually linked to impaired surfactant secretion and reutilization [5,7,8].
From alveolar lamellar body-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does a candidate gene regulate lamellar body biogenesis? | CRISPR knockout in mouse alveolar epithelial cells |
| Does autophagy contribute to lamellar body formation? | Autophagy gene perturbation in type 2 alveolar epithelial cells |
| How is surfactant protein B trafficked to the lamellar body? | Tagged knock-in of SFTPB in alveolar type II cells |
| Do Rab3D and actin define lamellar body subpopulations? | Knockout or point mutation of RAB3D in alveolar epithelial type II cells |
| Is lamellar body membrane turnover secretagogue-responsive? | Overexpression or knockout models with secretagogue stimulation |
| How do lamellar body hydrolases change during injury? | Ozone-induced alveolar injury model with hydrolase assays [3,6] |
How to Study the alveolar lamellar body Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Electron microscopy | Lamellar body morphology and responses | Alveolar injury and repair models |
| Fluorescence imaging of Rab3D and actin | Lamellar body subpopulations | Alveolar epithelial type II cells |
| Cargo trafficking assays for SFTPB | Delivery of surfactant protein B to lamellar body | Type II cell trafficking studies |
| Hydrolase enzyme assays | Sequential changes in lamellar body hydrolases | Ozone-induced injury and repair |
| Secretagogue stimulation assays | Lamellar body membrane turnover | Regulated secretion studies |
| Genetic perturbation of GCN5L1 | Lamellar body biogenesis and trafficking | Mouse alveolar epithelial cells |
| Autophagy perturbation | Lamellar body formation and surfactant production | Type 2 alveolar epithelial cells |
| Surfactant production measurement | Pulmonary surfactant output | Functional readout of lamellar body activity [1,4] |
Imaging Lamellar Bodies
Electron microscopy and related imaging approaches have been used to visualize lamellar body responses in rat models of alveolar injury and repair. Imaging of Rab3D and actin has revealed distinct lamellar body subpopulations in alveolar epithelial type II cells, demonstrating the value of fluorescence-based methods for organelle heterogeneity. Trafficking of newly synthesized surfactant protein B to the lamellar body has also been studied by tracking cargo in alveolar type II cells.
Biochemical and Enzymatic Assays
Sequential changes of lamellar body hydrolases during ozone-induced alveolar injury and repair were measured biochemically, providing a template for enzymatic profiling of the organelle. Lamellar body membrane turnover stimulated by secretagogues can be assessed through membrane trafficking assays. These approaches quantify the dynamic content and membrane behavior of the organelle [3,7].
Genetic Perturbation and Functional Readouts
GCN5L1 regulation of pulmonary surfactant production has been studied by modulating lamellar body biogenesis and trafficking in mouse alveolar epithelial cells. Autophagy contribution to lamellar body formation and surfactant production has been tested by perturbing autophagy in type 2 alveolar epithelial cells. Such genetic approaches allow causal testing of candidate genes in organelle biology [1,2].
Injury and Repair Models
Ozone-induced alveolar injury and repair models have been used to track lamellar body responses over time. These models, combined with hydrolase measurements, reveal sequential changes in the organelle during damage and recovery. They are useful for linking lamellar body biology to epithelial regeneration [3,6].
How CRISPR Can Be Used to Study GO:0097208 alveolar lamellar body
Knockout
CRISPR knockout of candidate genes such as GCN5L1 in mouse alveolar epithelial cells can test whether the gene is required for lamellar body biogenesis and trafficking. Knockout of autophagy-related genes in type 2 alveolar epithelial cells can test the contribution of autophagy to lamellar body formation and surfactant production. Knockout of RAB3D in alveolar epithelial type II cells can probe the role of Rab3D in defining lamellar body subpopulations.
Point Mutation
Point mutations can be introduced into genes such as RAB3D to dissect domain-specific functions in lamellar body subpopulation organization. Point mutations in trafficking regulators can test whether specific residues are required for lamellar body biogenesis and trafficking. Such models complement knockout approaches by separating loss of function from loss of protein [1,8].
Knock-in
Tagged knock-in of SFTPB allows visualization of newly synthesized surfactant protein B trafficking to the lamellar body in alveolar type II cells. Knock-in of fluorescent or epitope tags into lamellar body-associated genes can enable live-cell tracking of organelle dynamics [5,8]. These models are valuable for studying cargo delivery and organelle heterogeneity [5,8].
Overexpression
Overexpression of GCN5L1 or related regulators can test whether increased dosage alters lamellar body biogenesis and surfactant production. Overexpression of autophagy-related genes can probe whether enhanced autophagy promotes lamellar body formation and surfactant production. Overexpression studies complement loss-of-function models to establish sufficiency in organelle biology [1,2].
How EDITGENE Supports alveolar lamellar body Research
Researchers studying alveolar lamellar body-related genes often need to determine whether a candidate gene is causally involved in organelle biogenesis, cargo trafficking, or regulated secretion, and CRISPR-based models provide a direct route to that causal test [1,2,5,8].
Contact EDITGENE today to design your custom CRISPR model for alveolar lamellar body research.
Related Products
| Product name | Cat.No. | Species | Gene ID | |
|---|---|---|---|---|
| CTSH Knockout HEK293 Cell Line | EDJ-KQ2158 | Human | 1512 | Details Get a Quote |
| SFTPB Knockout HEK293 Cell Line | EDJ-KQ2276 | Human | 6439 | Details Get a Quote |
| ABCA3 Knockout HEK293 Cell Line | EDJ-KQ3344 | Human | 21 | Details Get a Quote |
| SFTPC Knockout HEK293 Cell Line | EDJ-KQ3915 | Human | 6440 | Details Get a Quote |
| ANXA7 Knockout HEK293 Cell Line | EDJ-KQ4057 | Human | 310 | Details Get a Quote |
| NAPSA Knockout HEK293 Cell Line | EDJ-KQ6600 | Human | 9476 | Details Get a Quote |
| ABCA3 Knockout A-549 Cell Line | EDJ-KQ24988 | Human | 21 | Details Get a Quote |
| ABCA3 Knockout HCT 116 Cell Line | EDJ-KQ24989 | Human | 21 | Details Get a Quote |
| ABCA3 Knockout HeLa Cell Line | EDJ-KQ24990 | Human | 21 | Details Get a Quote |
| CTSH Knockout A-549 Cell Line | EDJ-KQ22355 | Human | 1512 | Details Get a Quote |
| CTSH Knockout HCT 116 Cell Line | EDJ-KQ22356 | Human | 1512 | Details Get a Quote |
| CTSH Knockout HeLa Cell Line | EDJ-KQ22357 | Human | 1512 | Details Get a Quote |
| ANXA7 Knockout A-549 Cell Line | EDJ-KQ26418 | Human | 310 | Details Get a Quote |
| ANXA7 Knockout HCT 116 Cell Line | EDJ-KQ26419 | Human | 310 | Details Get a Quote |
| ANXA7 Knockout HeLa Cell Line | EDJ-KQ26420 | Human | 310 | Details Get a Quote |
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Frequently Asked Questions About alveolar lamellar body
What is the alveolar lamellar body (GO:0097208)?
The alveolar lamellar body is a specialized secretory organelle found in type II pneumocytes and involved in the synthesis, secretion, and reutilization of pulmonary surfactant.
What genes are involved in alveolar lamellar body biology?
Genes and proteins linked to lamellar body biology include GCN5L1, autophagy-related genes, SFTPB, RAB3D, and actin, among others [1,2,5,8].
How is the alveolar lamellar body formed?
Lamellar body formation involves autophagy-related membrane pathways and is regulated by GCN5L1 in mouse alveolar epithelial cells [1,2].
What is the function of the alveolar lamellar body?
Its major function is the synthesis, storage, secretion, and reutilization of pulmonary surfactant.
Which cell type contains alveolar lamellar bodies?
Alveolar lamellar bodies are found in type II pneumocytes, also called alveolar epithelial type II cells [5,8].
How is surfactant protein B trafficked to the lamellar body?
Newly synthesized surfactant protein B is trafficked to the lamellar body in alveolar type II cells.
What happens to lamellar bodies during lung injury?
Ozone-induced alveolar injury causes lamellar body responses and sequential changes in lamellar body hydrolases during injury and repair [3,6].
Is lamellar body secretion regulated?
Yes, lamellar body membrane turnover is stimulated by secretagogues, indicating regulated secretion.
What markers define lamellar body subpopulations?
Rab3D and actin reveal distinct lamellar body subpopulations in alveolar epithelial type II cells.
How can CRISPR help study alveolar lamellar body genes?
CRISPR knockout, point mutation, knock-in, and overexpression models can test causal roles of genes in lamellar body biogenesis, trafficking, and secretion [1,2,5,8].
Conclusion
GO:0097208 alveolar lamellar body is a specialized secretory organelle of type II pneumocytes that governs the synthesis, secretion, and reutilization of pulmonary surfactant. Experimental studies have defined key regulatory inputs, including GCN5L1-dependent biogenesis and trafficking, autophagy-dependent formation, SFTPB cargo delivery, and Rab3D/actin-defined subpopulations [1,2,5,8]. The organelle also responds dynamically to alveolar injury and repair, as shown by ozone-induced changes in lamellar body hydrolases and lamellar body responses [3,6]. Together, these findings make the alveolar lamellar body a central cellular_component for lung biology research and a tractable target for CRISPR-based functional studies [1,2,5,7].
References
- 1. Xu W et al.. 2023. GCN5L1 regulates pulmonary surfactant production by modulating lamellar body biogenesis and trafficking in mouse alveolar epithelial cells.. Cell Mol Biol Lett 28(1):90 PMID: 37936104
- 2. Li X et al.. 2022. The Role of Autophagy in Lamellar Body Formation and Surfactant Production in Type 2 Alveolar Epithelial Cells.. Int J Biol Sci 18(3):1107-1119 PMID: 35173542
- 3. Glew RH et al.. 1989. Sequential changes of lamellar body hydrolases during ozone-induced alveolar injury and repair.. Am J Pathol 134(5):1143-50 PMID: 2719079
- 4. Jobe AH et al.. 1993. Surfactant metabolism.. Clin Perinatol 20(4):683-96 PMID: 8131362
- 5. Osanai K et al.. 2020. Trafficking of newly synthesized surfactant protein B to the lamellar body in alveolar type II cells.. Cell Tissue Res 381(3):427-438 PMID: 32556725
- 6. Balis JU et al.. 1988. Ozone-induced lamellar body responses in a rat model for alveolar injury and repair.. Am J Pathol 132(2):330-44 PMID: 3400776
- 7. Bates SR et al.. 2000. Lamellar body membrane turnover is stimulated by secretagogues.. Am J Physiol Lung Cell Mol Physiol 278(3):L443-52 PMID: 10710515
- 8. van Weeren L et al.. 2004. Rab3D and actin reveal distinct lamellar body subpopulations in alveolar epithelial type II cells.. Am J Respir Cell Mol Biol 30(3):288-95 PMID: 12933357
