Target intelligence / Profile preview

Kinesin family member 2A (KIF2A)

Target
KIF2A
Molecular classification
Motor protein, Kinesin superfamily protein, Microtubule depolymerase, Enzyme (regulatory, not classical hydrolase/kinase), Other (structural/mitotic regulator)
01

Overview

Kinesin family member 2A (KIF2A) is a microtubule depolymerase belonging to the kinesin-13 family. It plays a critical role in the regulation of microtubule dynamics, particularly during mitosis, by disassembling microtubules at spindle poles, enabling proper spindle assembly, chromosome alignment, and segregation. KIF2A is also involved in neuronal morphogenesis. Dysregulated or aberrant expression of KIF2A functions as an oncoprotein, promoting proliferation, invasion, and chemoresistance in several cancers by activating PI3K/AKT, VEGF, Wnt, and Notch signaling pathways. High levels of KIF2A associate with increased tumor size, higher pathologic stage, and poor prognosis. No direct drugs currently target KIF2A, but its modulation alters the response to microtubule-targeting and DNA-damaging chemotherapies. As KIF2A is essential for both mitotic regulation and neuronal development, targeting it therapeutically is challenging and associated with potential safety concerns[1][2][3][4][5].

Other names
Kinesin-like protein KIF2AKIF2KNS2hK2HK2Kinesin-2CDCBM3kinesin heavy chain member 2AKinesin, heavy chain, 2kinesin-2
02

Mechanism of action

Modulation of microtubule depolymerization affects cancer cell sensitivity to DNA damage and microtubule-targeting agents. Regulates the PI3K/AKT/VEGF and Wnt/Notch signaling pathways, impacting malignant behaviors and drug resistance.

03

Biological functions

Regulation of microtubule assemblySpindle organizationChromosome congression and segregationCell cycle progression (mitosis)Neuronal development (neuron branch extension)Regulation of cell division
04

Disease associations

Cancer (oncoprotein in multiple solid tumors, e.g., lung, oral squamous carcinoma)Neurodevelopmental disorders (e.g., mutations can cause congenital fibrosis of extraocular muscles type 3)
05

Safety considerations

Potential disruption of normal mitosis and neuronal development if systemically inhibitedOff-target effects on microtubule function in non-cancerous rapidly dividing cellsLimited therapeutic index due to essential roles in normal cell division
06

Interacting drugs

Cisplatin

1 more in the full profile.

07

Biomarkers

KIF2A expression (high expression is a biomarker for greater tumor size, higher invasion/metastasis, poor prognosis in several cancers)

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