海角破解版

Nocodazole

Microtubule polymerization inhibitor; Inhibits beta-tubulin

Nocodazole

Microtubule polymerization inhibitor; Inhibits beta-tubulin

Catalog #
(Select a product)
Microtubule polymerization inhibitor; Inhibits beta-tubulin
Request Pricing Request Pricing

Overview

Nocodazole is an anti-mitotic agent that reversibly interferes with the polymerization of microtubules
(De Brabander et al.). Nocodazole binds to beta-tubulin and disrupts microtubule assembly/disassembly dynamics, impairing formation of the metaphase spindles during the cell division cycle. This prevents mitosis by inducing a G2/M-phase arrest and induces apoptosis in tumor cells (Jordan et al.).


GENOME EDITING
路 Synchronizes human pluripotent stem cells (hPSCs) in the G2/M cell cycle phase, thereby increasing the efficiency of homology-directed repair (HDR) in CRISPR-Cas9 genome editing (Lin et al.; Yang et al.).

CANCER RESEARCH
路 Induces apoptosis in leukemic cells without harming T cells and/or mesenchymal stromal cells that were recovered from the same patients (Frezzato et al.).
Cell Type
Cancer Cells and Cell Lines, Leukemia/Lymphoma Cells, Pluripotent Stem Cells
Species
Human, Mouse, Non-Human Primate, Other, Rat
Application
Genome Editing
Area of Interest
Cancer, Stem Cell Biology
CAS Number
31430-18-9
Chemical Formula
颁鈧佲倓贬鈧佲倎狈鈧僌鈧侨
Purity
鈮 98%

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Document Type
Product Name
Catalog #
Lot #
Language
Document Type
Product Name
Catalog #
74074, 74072
Lot #
All
Language
English
Document Type
Product Name
Catalog #
74074, 74072
Lot #
All
Language
English

Applications

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Research Area
Workflow Stages
Workflow Stages for Genome Editing

Resources and Publications

Publications (1)

Matrix stiffness drives drop like nuclear deformation and lamin A/C tension-dependent YAP nuclear localization T. Wang et al. Nature Communications 2024 Nov

Abstract

Extracellular matrix (ECM) stiffness influences cancer cell fate by altering gene expression. Previous studies suggest that stiffness-induced nuclear deformation may regulate gene expression through YAP nuclear localization. We investigated the role of the nuclear lamina in this process. We show that the nuclear lamina exhibits mechanical threshold behavior: once unwrinkled, the nuclear lamina is inextensible. A computational model predicts that the unwrinkled lamina is under tension, which is confirmed using a lamin tension sensor. Laminar unwrinkling is caused by nuclear flattening during cell spreading on stiff ECM. Knockdown of lamin A/C eliminates nuclear surface tension and decreases nuclear YAP localization. These findings show that nuclear deformation in cells conforms to the nuclear drop model and reveal a role for lamin A/C tension in controlling YAP localization in cancer cells. Matrix stiffness induced nuclear deformation regulates gene expression. This study finds that cell spreading on a stiff matrix induces tension in the nuclear lamina which promotes nuclear localization of yes associated protein (YAP), a transcriptional co-activator.