RAB11A Human
Description
Cochlear Hair Cell Development
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RAB11A knockout in mice disrupts stereocilia bundle cohesion and kinocilium formation, leading to deafness .
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Facilitates apical protein trafficking (e.g., Ezrin, Syntaxin3) and planar cell polarity (PCP) signaling via Vangl2/Prickle-2 redistribution .
Endothelial Barrier Integrity
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Maintains vascular endothelial (VE)-cadherin at adherens junctions (AJs) by recycling endocytosed VE-cadherin, preventing lysosomal degradation .
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Rab11a depletion in endothelial cells increases basal permeability and impairs barrier recovery post-thrombin challenge, exacerbating sepsis-induced lung edema .
Cancer Progression
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In prostate cancer, RAB11A upregulation activates FAK/AKT signaling, driving proliferation, migration, and epithelial-mesenchymal transition (EMT) .
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FAK inhibitor PF562271 reverses RAB11A-mediated tumor growth in vitro and in vivo .
Associated Diseases
Therapeutic Potential
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Targeting RAB11A-mediated recycling pathways could restore endothelial barrier function in acute lung injury .
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Inhibition of RAB11A/FAK axis shows promise in prostate cancer therapy .
Research Tools and Antibodies
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Antibodies: Mouse monoclonal anti-RAB11A (Clone 918009) detects endogenous protein in human, mouse, and rat models .
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Knockout Models: Conditional Rab11a knockout mice exhibit hearing loss and stereocilia defects .
Future Directions
Product Specs
Q&A
FAQs on RAB11A Human in Academic Research
Advanced Research Questions
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How can researchers resolve contradictory findings about RAB11A’s role in apoptosis?
Conflicting data may arise due to cell type-specific effects. Methodological considerations: -
What experimental designs are optimal for studying RAB11A’s interaction with signaling pathways?
Focus on pathway crosstalk using:
Table 1: Rab11a in Gastric Cancer (Source: )
| Parameter | Rab11a Overexpression | Rab11a Knockdown |
|---|---|---|
| Cell proliferation rate | ↑ 1.8-fold | ↓ 40% |
| Invasion ability | ↑ 2.3-fold | ↓ 60% |
| Cisplatin-induced apoptosis | ↓ 15% | ↑ 35% |
Table 2: Rab11a in Breast Cancer (Source: )
| Parameter | Wild-Type Rab11a | Dominant-Negative Rab11a |
|---|---|---|
| EGFR recycling rate | Accelerated | Abolished |
| EGF-induced motility | No change | ↑ 2.1-fold |
Methodological Guidance
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How to model RAB11A-mediated viral genome transmission?
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What bioinformatics tools are essential for analyzing RAB11A genomic data?
Addressing Technical Challenges
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How to ensure recombinant RAB11A protein functionality in vitro?
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What controls are critical in Rab11a siRNA experiments?
Product Science Overview
RAB11A is a gene that encodes a protein belonging to the Rab family of small GTPases. These proteins are key regulators of intracellular membrane trafficking, which includes the formation of transport vesicles and their fusion with target membranes. The RAB11A protein is involved in both constitutive and regulated secretory pathways and plays a crucial role in protein transport.
The RAB11A protein is a small GTPase that cycles between an inactive GDP-bound form and an active GTP-bound form. In its active form, it recruits various downstream effectors responsible for vesicle formation, movement, tethering, and fusion . Specifically, RAB11A regulates endocytic recycling, which is essential for maintaining cellular homeostasis and function .
RAB11A is involved in several cellular pathways, including:
- Vesicle-mediated transport: This pathway is crucial for the movement of molecules within cells.
- Aquaporin-mediated transport: This pathway involves the transport of water and small solutes across cell membranes .
RAB11A interacts with various proteins, including:
Mutations or dysregulation of the RAB11A gene have been associated with several diseases, including:
RAB11A is a subject of extensive research due to its critical role in intracellular trafficking and its implications in various diseases. Recombinant RAB11A protein is used in research to study its function, interactions, and potential therapeutic applications.
