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A mitotic inhibitor, microtubule inhibitor, or tubulin inhibitor, is a drug that inhibits mitosis, or cell division, and is used in treating cancer, gout, and nail fungus. These drugs disrupt microtubules , which are structures that pull the chromosomes apart when a cell divides.
2.5 Histone deacetylase inhibitors: Panobinostat: add: add: add: add Romidepsin: IV: Histone deacetylase inhibitor, hence inducing alterations in gene expression in the affected cells. Peripheral and cutaneous T cell lymphoma. Electrolyte anomalies, anaemia, thrombocytopenia, neutropenia, lymphopenia and ECG anomalies. Valproate [Note 1] PO, IV ...
Thus, in essence, taxanes are mitotic inhibitors. In contrast to the taxanes, the vinca alkaloids prevent mitotic spindle formation through inhibition of tubulin polymerization. Both taxanes and vinca alkaloids are, therefore, named spindle poisons or mitosis poisons, but they act in different ways.
Monomethyl auristatin E is an antimitotic agent which inhibits cell division by blocking the polymerisation of tubulin.The linker to the monoclonal antibody is stable in extracellular fluid, but is cleaved by cathepsin once the conjugate has entered a tumor cell, thus activating the antimitotic mechanism.
Pages in category "Mitotic inhibitors" The following 32 pages are in this category, out of 32 total. This list may not reflect recent changes. ...
Early Mitotic Inhibitor 1 (EMI1) is an important cell cycle regulator which ensures timely mitotic entry by primarily inhibiting Anaphase-Promoting Complex/Cyclosome (APC/C) activity. This protein is present in many organisms including Xenopus, Zebrafish, Drosophila (homologous protein: Rca1), and Humans (also often known as F-box only protein ...
Mitotic exit is an important transition point that signifies the end of mitosis and the onset of new G1 phase for a cell, and the cell needs to rely on specific control mechanisms to ensure that once it exits mitosis, it never returns to mitosis until it has gone through G1, S, and G2 phases and passed all the necessary checkpoints.
This delay between cell-cell contact and onset of proliferation inhibition is shortened as the culture becomes more confluent. Thus, it may be reasonably concluded that cell-cell contact is an essential condition for contact inhibition of proliferation, but is by itself insufficient for mitotic inhibition.