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ArticleMolecular biology reports2025

Distribution analysis of RAB11A and RAB11B, small GTP-binding proteins, in mice.

Yumi Tsuneura, Tohru Matsuki, Shima Eda, Nanako Hamada, Akihiro Harada, Koh-Ichi Nagata, Atsuo Nakayama

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Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

7 authors.

Yumi TsuneuraDepartment of Cellular Pathology, Institute for Developmental Research, Aichi Developmental Disability Center, 713-8 Kamiya, Kasugai, 486-0392, Japan.
Tohru MatsukiDepartment of Cellular Pathology, Institute for Developmental Research, Aichi Developmental Disability Center, 713-8 Kamiya, Kasugai, 486-0392, Japan.
Shima EdaDepartment of Cellular Pathology, Institute for Developmental Research, Aichi Developmental Disability Center, 713-8 Kamiya, Kasugai, 486-0392, Japan.
Nanako HamadaDepartment of Molecular Neurobiology, Institute for Developmental Research, Aichi Developmental Disability Center, 713-8 Kamiya, Kasugai, 480-0392, Japan.
Akihiro HaradaDepartment of Cell Biology, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, 565-0871, Japan.
Koh-Ichi NagataDepartment of Molecular Neurobiology, Institute for Developmental Research, Aichi Developmental Disability Center, 713-8 Kamiya, Kasugai, 480-0392, Japan.
Atsuo NakayamaDepartment of Cellular Pathology, Institute for Developmental Research, Aichi Developmental Disability Center, 713-8 Kamiya, Kasugai, 486-0392, Japan. atsuon@inst-hsc.jp.

Funding

Japan Society for the Promotion of Science JP20K08224Japan Society for the Promotion of Science JP22K15912
6 · The paper itself

Abstract

backgroundRAB11 is a small GTP-binding protein that regulates intracellular trafficking of recycling endosomes and is thereby involved in several neural functions. Highly similar RAB11 isoforms are encoded by RAB11A and RAB11B genes, and their pathogenic variants are associated with similar neurodevelopmental disorders, suggesting that RAB11A and RAB11B play similar and important roles in brain development. However, the detailed distribution patterns of these isoforms in various organs, including the brain, remain undetermined. METHODS AND

resultsWe generated an antibody against RAB11A and analyzed the distribution of RAB11A and RAB11B in mice. RAB11A was highly expressed in the ovary and the uterus but less abundant in the brain, whereas RAB11B was abundant in the brain, the testis, the ovary, and the uterus. In the developing cortex, RAB11A was enriched in the apical endfeet of apical radial glial cells, whereas RAB11B was abundantly expressed in postmigratory neurons of the cortical plate. In the adult mouse brain, RAB11A and RAB11B were similarly expressed in most neurons, with weak RAB11A signals also observed in the neuropil. In cultured neurons, RAB11A and RAB11B showed only partial co-localization and differential distribution in both soma and neurites. Notably, RAB11A appeared to be more abundant at presynapses than RAB11B.

conclusionsRAB11A and RAB11B exhibit distinct and characteristic distributions in the brain and other organs, suggesting they play different roles throughout the body. In particular, our results suggest they make distinct contributions to cortical development and regulation of the synaptic vesicle cycle.

Indexed as

rab GTP-Binding ProteinsAnimalsBrainFemaleMaleMiceMice, Inbred C57BLNeuronsOvaryrab11 GTP-Binding ProteinsUterusrab11 GTP-Binding Proteinsrab GTP-Binding ProteinsApical radial glial cellBrain developmentNeuronRAB11ARAB11BSynaptic vesicle

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.