| + |
APC-c | down-regulates quantity by destabilization 
ubiquitination
|
KIF18A |
0.302 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266110 |
|
|
in vitro |
|
| pmid |
sentence |
| 24510915 |
Biochemical studies on the kinesins confirmed KIFC1, KIF18A, KIF2C, and KIF4A as APC/C substrates. Furthermore, we showed that the APC/CCDH1-dependent degradation of KIFC1 regulates the bipolar spindle formation and proper cell division. Our in vitro degradation assays showed a time-dependent degradation for four of the five potential substrates tested: KIF18A, KIF2C, KIFC1 and KIF4A were readily degraded in vitro, however remained stable in the presence of either APC/C inhibitor (Fig(Fig4A4A and Supplementary Fig S3A). |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
KIF18A | up-regulates 
|
Plus-end directed sliding movement |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272526 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19773780 |
In general, N-kinesins and C-kinesins drive microtubule plus end- and minus end-directed motilities, respectively, and M-kinesins depolymerize microtubules1,9 (Box 1).|Forty-five genes that encode kinesin superfamily proteins (also known as KIFs) have been discovered in the mouse and human genomes.|KIFs are molecular motors that directionally transport various cargos, including membranous organelles, protein complexes and mRNAs, along the microtubule system. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
KIF18A
- 
- 