High impact information on CIN1

• Systematic mutational testing and transcriptional profiling of CIN candidate kinetochore genes should shed light on the kinetochore's role in tumorigenesis, and on the general role CIN plays in cancer development [1].
• A dysfunctional kinetochore represents one possible source for chromosome instability (CIN) and the generation of aneuploidy [1].
• Our findings suggest that the CIN1, CIN2, and CIN4 proteins contribute to microtubule stability either by regulating the activity of a yeast microtubule component or as structural components of microtubules [2].
• Overproduction of the CIN1 gene product was found to cause the same phenotype as loss of function, supersensitivity to benomyl [2].
• The role of this distinct difference was studied by substituting the proline residue of extracellular invertase CIN1 from Chenopodium rubrum with a valine residue, by site-directed mutagenesis [3].

Biological context of CIN1

• Significantly, excess Cin1p/cofactor D suppresses the conditional phenotypes of that mutant alpha-tubulin [4].
• At 11 degrees C, cin mutants arrest at the mitosis stage of their cell cycle because of loss of most microtubule structure. cin1, cin2, and cin4 mutations also cause defects in two other microtubule-mediated processes, nuclear migration and nuclear fusion (karyogamy) [2].
• We discovered and sequenced two complete retrotransposons of this family, and named them Cinful elements because they are members of a family of maize retrotransposons including Zeon-1 and the first plant transposable element sequenced, the solo long terminal repeat (LTR) called Cin1 [5].

Anatomical context of CIN1

• Saccharomyces cerevisiae PAC2 functions with CIN1, 2 and 4 in a pathway leading to normal microtubule stability [6].

Associations of CIN1 with chemical compounds

• Our findings suggest that the guanine nucleotide-binding Cin4p interacts with Cin1p and regulates its tubulin folding activity [6].

Other interactions of CIN1

• The products of the Saccharomyces cerevisiae CIN1, CIN2 and CIN4 genes participate in a nonessential pathway required for normal microtubule function [6].

References