Publications by authors named "N Raich"

spp. may cause opportunistic infections called vulvovaginal candidiasis (VVC), which is estimated to be the second most common cause of vaginitis worldwide. Under various circumstances, VVC could compromise pregnancy outcomes.

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Drosophila testes are a powerful model system for studying biological processes including stem cell biology, nuclear architecture, meiosis and sperm development. However, immunolabeling of the whole Drosophila testis is often associated with significant non-uniformity of staining due to antibody penetration. Squashed preparations only partially overcome the problem since it decreases the 3D quality of the analyses.

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The Mad1 spindle checkpoint protein helps organize several nucleoplasmic components, and flies lacking Mad1 present changes in gene expression reflecting altered chromatin conformation. In interphase, checkpoint protein Mad1 is usually described as localizing to the inner nuclear envelope by binding the nucleoporin Tpr, an interaction believed to contribute to proper mitotic regulation. Whether Mad1 has other nuclear interphase functions is unknown.

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Article Synopsis
  • The activity of Mad1 at kinetochores is crucial for the spindle assembly checkpoint (SAC), which prevents anaphase from starting if kinetochores aren't properly attached to spindle fibers.
  • The RZZ complex (Rod, Zw10, Zwilch) is key for recruiting Mad1 to kinetochores, but how this happens isn't fully understood.
  • This study shows that while Mad1 has a dynamic presence at unattached kinetochores with a half-life of 12 seconds, RZZ remains stable, and there's a physical association between Mad1 and RZZ.
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In the treatment of colon cancer, the development of resistance to apoptosis is a major factor in resistance to therapy. New molecular approaches to overcome apoptosis resistance, such as selectively upregulating proapoptotic proteins, are needed in colon cancer therapy. In a mouse model with inactivation of the adenomatous polyposis coli (Apc) tumor suppressor gene, reflecting the pathogenesis of most human colon cancers, the gene encoding feminization-1 homolog b (Fem1b) is upregulated in intestinal epithelium following Apc inactivation.

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