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Related Concept Videos

Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
Cell Polarization by Rho Proteins01:21

Cell Polarization by Rho Proteins

Cell polarity is the asymmetric distribution of cellular and membrane components, making one side of the cell different from the other. This polarity is essential to many processes such as embryogenesis, axon migration, glucose transport across epithelial cells, and directional cell migration. A migrating cell responds to intracellular or extracellular signals via molecular cascades that reorganize the actin cytoskeleton to establish this polarity. In these cells, the Rho family proteins Cdc42,...
Mechanism of Lamellipodia Formation01:31

Mechanism of Lamellipodia Formation

Cells migrating in response to external stimuli form lamellipodia, which are thin membrane protrusions supported by a mesh of linked, branched, or unbranched actin filaments. These actin filaments interact with myosin motor proteins, creating the dynamic actomyosin complex within the cytoskeleton. Contractility, or the ability to generate contractile stress, is inherent to the actomyosin complex. It helps cells detect the stiffness of the surrounding ECM and exert contractile force for...
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
Microtubule Associated Proteins (MAPs)01:42

Microtubule Associated Proteins (MAPs)

Microtubule function and architecture are regulated by an array of specialized proteins called microtubule-associated proteins or MAPs. These proteins are widespread across different organisms and have conserved protein motifs, like the multi-TOG domain for tubulin binding found in the CLASP family of MAPs. Some MAPs are lineage-specific based on their conserved domains. Their functions depend upon the cytoskeletal architecture and cell type they are located within. In-plant cells, a specific...
Cytoskeletal Coordination in Cell Migration01:32

Cytoskeletal Coordination in Cell Migration

A migrating cell changes its shape during the cyclic events of attachment and detachment from the substratum and repositions the cell organelles correspondingly. These complex events are orchestrated by the dynamic cytoskeletal network comprising actin filaments, intermediate filaments, and microtubules. Cytoskeletal crosstalk — the direct and indirect communication between the different components — is crucial for this coordination. Direct communication involves various linker proteins that...

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Related Experiment Video

Updated: Jun 10, 2026

Genetic Manipulation of Cerebellar Granule Neurons In Vitro and In Vivo to Study Neuronal Morphology and Migration
09:07

Genetic Manipulation of Cerebellar Granule Neurons In Vitro and In Vivo to Study Neuronal Morphology and Migration

Published on: March 17, 2014

MAP1B regulates axonal development by modulating Rho-GTPase Rac1 activity.

Carolina Montenegro-Venegas1, Elena Tortosa, Silvana Rosso

  • 1Department of Biology, Universidad de Chile, Santiago, Chile.

Molecular Biology of the Cell
|August 20, 2010
PubMed
Summary
This summary is machine-generated.

Microtubule-associated protein 1B (MAP1B) is crucial for neuronal development. MAP1B deficiency impairs axon growth by disrupting Rac1/cdc42 signaling, a defect rescued by restoring Rac1 or cdc42 activity.

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Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells
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Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells

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Analyses of Actin Dynamics, Clutch Coupling and Traction Force for Growth Cone Advance
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Analyses of Actin Dynamics, Clutch Coupling and Traction Force for Growth Cone Advance

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Related Experiment Videos

Last Updated: Jun 10, 2026

Genetic Manipulation of Cerebellar Granule Neurons In Vitro and In Vivo to Study Neuronal Morphology and Migration
09:07

Genetic Manipulation of Cerebellar Granule Neurons In Vitro and In Vivo to Study Neuronal Morphology and Migration

Published on: March 17, 2014

Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells
10:27

Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells

Published on: March 9, 2012

Analyses of Actin Dynamics, Clutch Coupling and Traction Force for Growth Cone Advance
07:53

Analyses of Actin Dynamics, Clutch Coupling and Traction Force for Growth Cone Advance

Published on: October 21, 2021

Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Microtubule-associated protein 1B (MAP1B) plays a role in neuronal development.
  • MAP1B-deficient neurons exhibit delayed axon outgrowth and reduced axonal elongation compared to wild-type neurons.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which MAP1B influences axon growth.
  • To investigate the role of MAP1B in regulating small GTPase signaling pathways.

Main Methods:

  • Utilized MAP1B-deficient mouse models.
  • Assessed the activity of Rho GTPases (Rac1, cdc42, Rho) in cultured neurons.
  • Performed co-immunoprecipitation to identify interacting proteins.
  • Analyzed the phosphorylation status of downstream effectors like LIMK-1 and cofilin.
  • Employed rescue experiments using constitutively active forms of Rac1, cdc42, and Tiam1.

Main Results:

  • MAP1B deficiency led to decreased Rac1 and cdc42 activity, and increased Rho activity.
  • MAP1B was found to interact with Tiam1, a guanine nucleotide exchange factor for Rac1.
  • Reduced Rac1/cdc42 activity correlated with decreased phosphorylation of LIMK-1 and cofilin.
  • Overexpression of active Rac1, cdc42, or Tiam1 rescued the axon growth defect in MAP1B-deficient neurons.

Conclusions:

  • MAP1B is essential for maintaining proper Rac1 and cdc42 activity during neuronal development.
  • MAP1B facilitates communication between microtubules and the actin cytoskeleton.
  • MAP1B's interaction with Tiam1 is critical for regulating downstream signaling pathways involved in axon growth.
  • These findings reveal a novel function of MAP1B in neuronal polarization and axonogenesis.