Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.4.4 (kinesin)
 5,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recently, kinesin motor proteins have been focused on as targets for cancer therapy. Kinesins are microtubule-based motor proteins that mediate diverse functions within the cell, including the transport of vesicles, organelles, chromosomes and protein complexes, as well as the movement of microtubules. In the current study, the expression of kinesin family member 18A (KIF18A), a member of kinesin superfamily, was investigated in breast cancer using immunohistochemistry, and its effect on breast cancer prognosis was examined. KIF18A expression level was significantly associated with lymph node metastasis (P=0.047). In patients with high levels of KIF18A expression, survival was significantly poorer compared to patients with low levels of KIF18A expression (disease-free survival, P=0.030). Multivariate analysis revealed that venous invasion (hazard ratio, 9.22; 95% confidence interval, 3.90-23.66; P<0.001) and KIF18A expression (hazard ratio, 3.20; 95% confidence interval, 1.34-6.09; P=0.010) were independent predictive factors for lymph node metastasis. KIF18A may be a useful predictive marker for lymph node metastasis in breast cancer, which could facilitate curative adjuvant treatment.
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PMID:Clinicopathological relevance of kinesin family member 18A expression in invasive breast cancer. 2758 39

The influenza virus is one of the major public health threats. However, the development of efficient vaccines and therapeutic drugs to combat this virus is greatly limited by its frequent genetic mutations. Because of this, targeting the host factors required for influenza virus replication may be a more effective strategy for inhibiting a broader spectrum of variants. Here, we demonstrated that inhibition of a motor protein kinesin family member 18A (KIF18A) suppresses the replication of the influenza A virus (IAV). The expression of KIF18A in host cells was increased following IAV infection. Intriguingly, treatment with the selective and ATP-competitive mitotic kinesin KIF18A inhibitor BTB-1 substantially decreased the expression of viral RNAs and proteins, and the production of infectious viral particles, while overexpression of KIF18A enhanced the replication of IAV. Importantly, BTB-1 treatment attenuated the activation of AKT, p38 MAPK, SAPK and Ran-binding protein 3 (RanBP3), which led to the prevention of the nuclear export of viral ribonucleoprotein complexes. Notably, administration of BTB-1 greatly improved the viability of IAV-infected mice. Collectively, our results unveiled a beneficial role of KIF18A in IAV replication, and thus, KIF18A could be a potential therapeutic target for the control of IAV infection.
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PMID:Selective and ATP-competitive kinesin KIF18A inhibitor suppresses the replication of influenza A virus. 3225 33