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(→Kinesin) |
(→Disease) |
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== Disease == | == Disease == | ||
| + | Kinesin is an important protein that aids with axon transport and cell division. If there is a mutation of the gene and/or a defect of the protein, then there can be transport of pathogens or defective roles relating to neural impulses and cell division. Therefore, there are many different consequences of a faulty kinesis. | ||
| + | |||
| + | Defective role in cell division: | ||
| + | |||
| + | 1. If kinesin cannot help regulate and aid cell division, then the cell can start dividing uncontrollably. Cancer cells take advantage of this to proliferate and grow rapidly. | ||
| + | |||
| + | 2. This can pose a threat to the organism, but if kinesin is causing rapid cell division, then it can be used as an identifiable target and treated with drugs. | ||
| + | |||
| + | Defective role in axon transport: | ||
| + | |||
| + | 1. A lot of environmental toxins can inactive kinesin and can no longer aid an axon in regards to transmitting neural signals. The motor functions of the human will start to deplete and will result in axonopathy (when nerves suddenly stop functioning). | ||
| + | |||
| + | 2. Diffusion is inefficient for long-distance transport which is one reason why there are action potentials in he nervous system and kinesin helps the axon transport signals. But when long-distance transport is being inhibited, then the human's nervous system starts to be malfunction and people can start showing symptoms similar to mayotrophic lateral sclerosis (ALS). | ||
== Relevance == | == Relevance == | ||
Revision as of 20:46, 21 February 2018
Contents |
Kinesin
Kinesins are ATP dependent motor proteins that perform intracellular transport along microtubules. Kinesin is a very important protein in meiosis as well as mitosis allowing for the mitotic spindles to separate. The movement along microtubules is commonly known as anterograde transport.
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Structure
This is a default text for your page '. Click above on edit this page' to modify. Be careful with the < and > signs. You may include any references to papers as in: the use of JSmol in Proteopedia [1] or to the article describing Jmol [2] to the rescue.
Function
Disease
Kinesin is an important protein that aids with axon transport and cell division. If there is a mutation of the gene and/or a defect of the protein, then there can be transport of pathogens or defective roles relating to neural impulses and cell division. Therefore, there are many different consequences of a faulty kinesis.
Defective role in cell division:
1. If kinesin cannot help regulate and aid cell division, then the cell can start dividing uncontrollably. Cancer cells take advantage of this to proliferate and grow rapidly.
2. This can pose a threat to the organism, but if kinesin is causing rapid cell division, then it can be used as an identifiable target and treated with drugs.
Defective role in axon transport:
1. A lot of environmental toxins can inactive kinesin and can no longer aid an axon in regards to transmitting neural signals. The motor functions of the human will start to deplete and will result in axonopathy (when nerves suddenly stop functioning).
2. Diffusion is inefficient for long-distance transport which is one reason why there are action potentials in he nervous system and kinesin helps the axon transport signals. But when long-distance transport is being inhibited, then the human's nervous system starts to be malfunction and people can start showing symptoms similar to mayotrophic lateral sclerosis (ALS).
Relevance
Structural highlights
This is a sample scene created with SAT to by Group, and another to make of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.
</StructureSection>
References
- ↑ Hanson, R. M., Prilusky, J., Renjian, Z., Nakane, T. and Sussman, J. L. (2013), JSmol and the Next-Generation Web-Based Representation of 3D Molecular Structure as Applied to Proteopedia. Isr. J. Chem., 53:207-216. doi:http://dx.doi.org/10.1002/ijch.201300024
- ↑ Herraez A. Biomolecules in the computer: Jmol to the rescue. Biochem Mol Biol Educ. 2006 Jul;34(4):255-61. doi: 10.1002/bmb.2006.494034042644. PMID:21638687 doi:10.1002/bmb.2006.494034042644
