PubMed Health⌕ Search

Biomedical subjects

Tatsuyoshi Yamamoto

Publications and source records attributed to Tatsuyoshi Yamamoto.

3 recordsLinked to original sources

Novel development rescuing factors (DRFs) secreted by the developing Dictyostelium cells, that are involved in the restoration of a mutant lacking MAP-kinase ERK2.

We found novel development rescuing factors (DRFs) secreted from developing Dictyostelium cells, by using a mutant (erkB-) which is missing MAP-kinase ERK2 as a test strain for bioassay. The mutant erkB- fails to undergo multicellular morphogenesis due to impaired cAMP signaling. However, such developmental defect can be restored by the presence of low-molecular weight DRFs that are secreted from developing wild-type cells. We previously showed that DIF-1 (Differentiation-Inducing Factor 1 for stalk cells) possesses this activity, indicating a newly discovered role of DIF-1. Surprisingly, however, the mutant dmtA-, which is incapable of DIF-1 synthesis still exerts a strong inducing activity of the multicellular morphogenesis of erkB-. After analysis of HPLC fractions of conditioned media prepared from both wild type Ax2 and dmtA- strains revealed that both strains secrete at least two novel DRF activities with DIF-like mobility. However, these activities were not derived from other DIFs such as DIF-2 and DIF-3. Identification of these DRFs found in this study would provide insight into the mechanism by which the development of the erkB- mutant is restored and how these factors act in the normal development of Dictyostelium.

Animals↗

Profiling of gene expression associated with hepatolithiasis by complementary DNA expression array.

By use of cDNA expression array method, we compared the expression profiles of genes in hepatolithiasis tissues with those of paired normal tissues. Expression of 1176 cancer related genes that include 33 tumor suppressor genes, 100 proto-oncogenes and 37 DNA damage repair genes were examined in this study. We found that expression of tumor suppressor genes and proto-oncogenes was systemically activated in hepatholithiasis tissues, suggesting that expression of genes controlling cell growth becomes unstable in liver lobe of hepatolithiasis. In contrast, expression of DNA damage repair genes were not activated but rather remained unchanged in hepatholithiasis tissues, suggesting that repair process is not strongly activated but rather impaired in hepatholithiasis tissues.

Calculi↗

Expression of p73 gene, cell proliferation and apoptosis in breast cancer: Immunohistochemical and clinicopathological study.

p73 is a member of p53 tumor suppressor protein family. In spite of similarities of three meaningful domains between p53 and p73, the exact function of p73 protein is not established. To approach the relevance of p73 expression to a pathological parameter in human breast cancer, the apoptotic index (AI) and the mitotic index (MI) were examined for 75 patients with the breast cancer after mastectomies. We found that both of the AI and MI in p73-positive cases were significantly higher compared to the p73-negative cases, suggesting that the p73-positive cases in the breast cancer were in advanced grade. In six cases of breast cancer with distant metastasis, however, the p73 expression was slight and showing low AI but high MI. Advanced breast cancer with distant metastasis seemed to lose the p73 expression and gain the function of evading apoptosis. Altogether, these data demonstrate that p73 expression is well correlated with AI in breast cancer.

Adenocarcinoma↗