Target intelligence / Profile preview

Kinesin family member 15 (KIF15)

Target
KIF15
Molecular classification
Motor protein, Microtubule-associated protein, Kinesin superfamily, Other
01

Overview

Kinesin family member 15 (KIF15) is a human motor protein from the kinesin superfamily, crucial for mitotic spindle assembly, chromosome segregation, and maintenance of spindle bipolarity during cell division[1][2][3][4]. KIF15 acts by cross-linking and sliding microtubules, generating forces that maintain spindle pole separation and support accurate segregation of chromosomes. It is highly expressed during mitosis and plays additional roles in neuronal development including axon and dendrite growth[1][2]. KIF15 is functionally redundant with KIF11/Eg5; if KIF11 is inhibited (such as by small-molecule drugs), upregulation of KIF15 can compensate, potentially leading to drug resistance[2][3]. Overexpression of KIF15 has been observed in various malignancies, correlating with enhanced tumor cell proliferation, migration, and resistance to certain cancer therapies[3][5][6]. Targeted KIF15 inhibition disrupts mitotic spindle function, reduces proliferation, and may increase cancer cell apoptosis, making it a therapeutic target, especially in combination strategies with KIF11 inhibitors[3].

Other names
Kinesin-like protein KIF15Kinesin-12HKLP2KNSL7NY-BR-62Kinesin-like protein 2Kinesin-like protein 7BRDCS2Serologically defined breast cancer antigen NY-BR-62KLP2hKLP2
02

Mechanism of action

Inhibition disrupts bipolar spindle formation, resulting in impaired mitosis and reduced proliferation of cancer cells[3]. Dual inhibition with KIF11/Eg5 may overcome resistance mechanisms and enhance anti-proliferative effects[2][3].

03

Biological functions

Cell division (mitosis)Microtubule organizationChromosome segregationIntracellular transportCell proliferationNeuronal development (axon growth, dendrite maturation)
04

Disease associations

Cancer (multiple types, including breast, pancreatic, gastric cancer, glioma)Other
05

Safety considerations

Functional redundancy with KIF11 suggests partial compensation if only one is inhibited, potentially requiring dual-target approaches[2][3]Essential role in mitosis may result in potential toxicity in rapidly dividing non-cancerous cells[3]
06

Interacting drugs

KIF15-IN-1

1 more in the full profile.

07

Biomarkers

Overexpression in tumor tissue (biomarker for poor prognosis in several cancers)[3][6]Candidate biomarker for glioma and triple-negative breast cancer[3][6]

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