scholarly journals Characterization of the KIF3C Neural Kinesin-like Motor from Mouse

1998 ◽  
Vol 9 (2) ◽  
pp. 249-261 ◽  
Author(s):  
Zhaohuai Yang ◽  
Lawrence S. B. Goldstein
Keyword(s):  
Spinal Cord ◽  
Axonal Transport ◽  
Intracellular Transport ◽  
Ganglion Cells ◽  
Double Labeling ◽  
Secondary Structure Analysis ◽  
Anterograde Axonal Transport ◽  
Brain Cdna Library ◽  
Kinesin Superfamily

Proteins of the kinesin superfamily define a class of microtubule-dependent motors that play crucial roles in cell division and intracellular transport. To study the molecular mechanism of axonal transport, a cDNA encoding a new kinesin-like protein called KIF3C was cloned from a mouse brain cDNA library. Sequence and secondary structure analysis revealed that KIF3C is a member of the KIF3 family. In contrast to KIF3A and KIF3B, Northern and Western analysis indicated that KIF3C expression is highly enriched in neural tissues such as brain, spinal cord, and retina. When anti-KIF3C antibodies were used to stain the cerebellum, the strongest signal came from the cell bodies and dendrites of Purkinje cells. In retina, anti-KIF3C mainly stains the ganglion cells. Immunolocalization showed that the KIF3C motor in spinal cord and sciatic nerve is mainly localized in cytoplasm. In spinal cord, the KIF3C staining was punctate; double labeling with anti-giantin and anti-KIF3C showed a clear concentration of the motor protein in the Golgi complex. Staining of ligated sciatic nerves demonstrated that the KIF3C motor accumulated at the proximal side of the ligated nerve, which suggests that KIF3C is an anterograde motor. Immunoprecipitation experiments revealed that KIF3C and KIF3A, but not KIF3B, were coprecipitated. These data, combined with previous data from other labs, indicate that KIF3C and KIF3B are “variable” subunits that associate with a common KIF3A subunit, but not with each other. Together these results suggest that KIF3 family members combinatorially associate to power anterograde axonal transport.

scholarly journals Molecular Cloning and Functional Analysis of Mouse C-Terminal Kinesin Motor KifC3

2001 ◽  
Vol 21 (3) ◽  
pp. 765-770 ◽  
Author(s):  
Zhaohuai Yang ◽  
Chun-hong Xia ◽  
Elizabeth A. Roberts ◽  
Kevin Bush ◽  
Sanjay K. Nigam ◽  
...  
Keyword(s):  
Knockout Mouse ◽  
Intracellular Transport ◽  
Normal Development ◽  
Embryonic Stem ◽  
Mouse Strains ◽  
General Role ◽  
Secondary Structure Analysis ◽  
Brain Cdna Library ◽  
Kinesin Superfamily

ABSTRACT Proteins of the kinesin superfamily define a class of microtubule-dependent motors that play crucial roles in cell division and intracellular transport. To study the molecular mechanism of intracellular transport involving microtubule-dependent motors, a cDNA encoding a new kinesin-like protein called KifC3 was cloned from a mouse brain cDNA library. Sequence and secondary structure analysis revealed that KifC3 is a member of the C-terminal motor family. In contrast to other mouse C-terminal motors, KifC3 is apparently ubiquitous and may have a general role in intracellular transport. To understand the in vivo function of the KifC3 gene, we used homologous recombination in embryonic stem cells to construct knockout mouse strains for the KifC3 gene. Homozygous mutants of theKifC3 gene are viable, reproduce normally, and apparently develop normally. These results suggest that KifC3 is dispensable for normal development and reproduction in the mouse.

Reduced axonal motor protein expression in non-lesional grey matter in multiple sclerosis

2013 ◽  
Vol 20 (7) ◽  
pp. 812-821 ◽  
Author(s):  
K Hares ◽  
K Kemp ◽  
C Rice ◽  
E Gray ◽  
N Scolding ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Protein Expression ◽  
Axonal Transport ◽  
Neurological Disease ◽  
Grey Matter ◽  
Messenger Ribonucleic Acid ◽  
Protein Levels ◽  
Anterograde Axonal Transport ◽  
Kinesin Superfamily ◽  
And Control

Background: Multiple sclerosis (MS) is a neurological disease characterised by central nervous system inflammation, demyelination, axonal degeneration and neuronal injury. Preventing neuronal and axon damage is of paramount importance in attempts to prevent disease progression. Intact axonal transport mechanisms are crucial to axonal integrity and evidence suggests these mechanisms are disrupted in MS. Anterograde axonal transport is mediated to a large extent through the kinesin superfamily proteins. Recently, certain kinesin superfamily proteins (KIF5A, KIF1B and KIF21B) were implicated in MS pathology. Objectives: To investigate the expression of KIF5A, KIF21B and KIF1B in MS and control post-mortem grey matter. Methods: Using both quantitative real-time polymerase chain reaction (PCR) and Immunodot-blots assays, we analysed the expression of kinesin superfamily proteins in 27 MS cases and 13 control cases not linked to neurological disease. Results: We have shown significant reductions in KIF5A, KIF21B and KIF1B messenger ribonucleic acid (mRNA) expression and also KIF5A protein expression in MS grey matter, as compared to control grey matter. Conclusion: We have shown significant reductions in mRNA and protein levels of axonal motor proteins in the grey matter of MS cases, which may have important implications for the pathogenesis of neuronal/axonal injury in the disease.

scholarly journals Functional Analysis of Mouse C-Terminal Kinesin Motor KifC2

2001 ◽  
Vol 21 (7) ◽  
pp. 2463-2466 ◽  
Author(s):  
Zhaohuai Yang ◽  
Elizabeth A. Roberts ◽  
Lawrence S. B. Goldstein
Keyword(s):  
Functional Analysis ◽  
Neural Development ◽  
Knockout Mouse ◽  
Intracellular Transport ◽  
Embryonic Stem ◽  
Mouse Strains ◽  
Secondary Structure Analysis ◽  
And Behavior ◽  
Kinesin Superfamily

ABSTRACT Proteins of the kinesin superfamily define a class of microtubule-dependent motors that play crucial roles in cell division and intracellular transport. In the mouse, several kinesin motors have been characterized and are suggested to play roles in axonal and/or dendritic transport. One such kinesin is KifC2. Sequence and secondary structure analysis revealed that KifC2 is a member of the C-terminal motor family. Northern and Western blot analyses indicated that KifC2 is specifically expressed in both the central and peripheral nervous systems. The cellular locations of the KifC2 proteins were found to be mainly in neural cell bodies and dendrites but also in axons. To understand the in vivo function of the KifC2 gene, we used homologous recombination in embryonic stem cells to construct knockout mouse strains for the KifC2 gene. HomozygousKifC2 mutants were viable and reproduced normally, and their development was apparently normal. These results suggest that KifC2 is dispensable for normal neural development and behavior in the mouse.

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