RAB7A
RAB7A (Ras-related protein Rab-7a, also known as RAB7 and CMT2B) is a small GTPase of the Rab family that regulates intracellular membrane trafficking. It governs endo-lysosomal transport, including the maturation of late endosomes and their delivery to lysosomes. Browse Assay Genie's current range of RAB7A research reagents below, or read on for the biology behind the target.
RAB7A belongs to the Rab family of the small GTPase superfamily. Like other Rabs, it cycles between an inactive GDP-bound form and an active GTP-bound form. In the active state it is recruited to membranes, where it binds a variety of effector proteins that act directly in vesicle formation, movement, tethering and fusion. Through these interactions RAB7A governs early-to-late endosomal maturation, microtubule minus-end and plus-end directed endosomal migration and positioning, and endosome-lysosome transport.
Beyond core endo-lysosomal trafficking, RAB7A has a central role in growth-factor-mediated cell signalling, nutrient uptake, neurotrophin transport in neuronal axons and lipid metabolism. It controls the endosomal trafficking and neurite outgrowth signalling of NTRK1/TRKA, and regulates the lysosomal degradation of the EGF-EGFR complex. It is also involved in specialised trafficking, including the maturation of melanosomes, autophagosomes and pathogen-induced phagosomes. It contributes to the maturation and acidification of phagosomes that engulf pathogens such as S. aureus and M. tuberculosis, and to their fusion with lysosomes. Other reported roles include ADRB2-stimulated lipolysis through lipophagy, the exosomal release of SDCBP, CD63 and syndecan, and vesicular trafficking and cell surface expression of ACE2. In concert with RAC1, it helps regulate ruffled border formation in osteoclasts.
The RAB7A gene is a member of the RAB, member RAS oncogene GTPases group, and its protein is found on phagosome, late endosome, lysosome, melanosome, autophagosome and mitochondrial membranes as well as lipid droplets. Mutations at highly conserved residues have caused some forms of Charcot-Marie-Tooth type 2 neuropathy, which explains the CMT2B alias. RAB7A is also involved in the cellular vacuolation caused by the VacA cytotoxin of Helicobacter pylori. Mouse and rat orthologs are both named Rab7a.
RAB7A governs early-to-late endosome maturation and endosome-lysosome transport, making it a core marker for studying late endocytic compartments.
RAB7A is involved in autophagosome maturation and in ADRB2-stimulated lipolysis through lipophagy, linking it to lipid metabolism research.
RAB7A mediates neurotrophin transport in axons and NTRK1 signalling, and its mutations cause some Charcot-Marie-Tooth type 2 neuropathies.
RAB7A contributes to phagosome maturation, acidification and lysosome fusion during infection by pathogens such as M. tuberculosis and S. aureus.
RAB7A is a small GTPase that regulates vesicle traffic in late endosomes and from late endosomes to lysosomes. In its active GTP-bound state it recruits effectors that control endosome maturation, positioning and transport, and it also supports autophagosome and phagosome maturation.
RAB7 is a previous symbol, and the gene was formerly named RAB7, member RAS oncogene family. CMT2B refers to Charcot-Marie-Tooth neuropathy 2B, because mutations at conserved residues in this gene have caused some forms of CMT type 2 neuropathy.
Yes. Mouse and rat both have an ortholog named Rab7a, so findings can often be compared across these species. Reactivity varies between reagents, so check the datasheet of any product for its validated reactivity.
Other Rab family GTPases and trafficking regulators involved in endocytic, recycling and secretory pathways.
Gene and protein annotations from HGNC, NCBI Gene and UniProt P51149; product specifications from Assay Genie datasheets.