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Literature summary for 2.1.1.233 extracted from

  • Xia, X.; Gholkar, A.; Senese, S.; Torres, J.Z.
    A LCMT1-PME-1 methylation equilibrium controls mitotic spindle size (2015), Cell Cycle, 14, 1938-1947.
    View publication on PubMedView publication on EuropePMC

Molecular Weight [Da]

Molecular Weight [Da] Molecular Weight Maximum [Da] Comment Organism
38000
-
x * 38000, SDS-PAGE Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Subunits

Subunits Comment Organism
? x * 38000, SDS-PAGE Homo sapiens

Synonyms

Synonyms Comment Organism
LCMT1
-
Homo sapiens
leucine carboxyl methyltransferase-1
-
Homo sapiens

General Information

General Information Comment Organism
malfunction depletion of leucine carboxyl methyltransferase-1, LCMT1, or overexpression of protein phosphatase methylesterase-1, PME-1, lead to long spindles. In contrast, depletion of PME-1, pharmacological inhibition of PME-1 or overexpression of LCMT1 lead to short spindles. Perturbation of the LCMT1-PME-1 methylation equilibrium leads to mitotic arrest, spindle assembly checkpoint activation, defective cell divisions, induction of apoptosis and reduced cell viability, phenotype, overview Homo sapiens
physiological function leucine carboxyl methyltransferase-1, LCMT1, and protein phosphatase methylesterase-1, PME-1, are essential enzymes that regulate the methylation of the protein phosphatase 2A catalytic subunit. The two enzymes have been linked to the regulation of cell growth and proliferation, and a role of LCMT1-PME-1 methylation equilibrium in controlling mitotic spindle size. The LCMT1-PME-1 methylation equilibrium is critical for regulating mitotic spindle size and thereby proper cell division Homo sapiens