EC Number   |
General Information |
Reference |
|---|
   5.6.1.3 | evolution |
conventional kinesin is the founding member of a superfamily of molecular motors that use the energy of ATP hydrolysis to transport cargo along microtubules, serving essential roles in a wide variety of cellular processes, most notably mitosis and neuronal transport |
733716 |
| 5.6.1.3 | evolution |
the enzyme belongs to the kinesin superfamily |
734310 |
| 5.6.1.3 | evolution |
the enzyme is a member of the kinesin-5 family |
732986 |
| 5.6.1.3 | evolution |
the enzyme is a mmember of the kinesin superfamily of molecular motors |
734241 |
| 5.6.1.3 | evolution |
the enzyme KIF4 belongs to the kinesin superfamily |
734474 |
| 5.6.1.3 | malfunction |
depletion of TbKIN-D disrupts cell morphology, resulting in elongation of the posterior of the cell, which is filled with newly assembled microtubules. RNAi of TbKIN-D impairs organelle segregation and leads to severe growth inhibition and cell death, TbKIN-D deficiency significantly interferes with cytoskeletal microtubules, phenotype |
734354 |
| 5.6.1.3 | malfunction |
disruptions in microtubule motor transport are associated with a variety of neurodegenerative diseases. Phosphorylation at serine 175/176 via c-Jun N-terminal kinase-3 is associated with Huntington disease and spinal and bulbar muscular atrophy |
734238 |
| 5.6.1.3 | malfunction |
disruptions in microtubule motor transport are associated with a variety of neurodegenerative diseases. Phosphorylation at serine 175/176 via c-Jun N-terminal kinase-3 is associated with Huntington disease and spinal and bulbar muscular atrophy. The ATPase, microtubule-binding affinity, and processivity are unchanged between a phosphomimetic S175D and a nonphosphorylatable S175A construct of kinesin. Placement of negative charge at Ser175, through phosphorylation or mutation, leads to a lower stall force and decreased velocity, addition of a negative charge at Ser175 favors the autoinhibited conformation of kinesin |
734238 |
| 5.6.1.3 | malfunction |
inhibition of Eg5 causes cell cycle arrest in mitosis with the irregular formation of monopolar spindles and subsequent apoptotic cell death |
732986 |
| 5.6.1.3 | metabolism |
a bias that favors motion toward the minus-end of microtubules might be used to tune transport in healthy cells when properly regulated but contribute to a disease state when misregulated |
734238 |
