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Aberrant expression of TSG101 in Taiwan Chinese breast cancer (2000)

Lo, Yung-Feng ; Chen, Tse-Ching ; Chen, Shin-Cheh ; [et al.]

Springer

Breast cancer research and treatment 60 (2000), S. 259-266

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ISSN: 1573-7217

Keywords: TSG101 ; breast cancer ; tumor suppressor

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Abstract Functional inactivation of the tsg101 gene in mouse fibroblasts results in cell transformation and the ability to form metastatic tumors in nude mice. The human tsg101 gene was mapped to chromosome 11q15.1-2 and found to mutate in some cancer patients. To test the expression pattern of the tsg101 gene in Chinese breast cancer patients, we analyzed the mRNA by RT-PCR in 51 breast cancer patients. The full-length tsg101 and 7 truncated transcripts were detected in both normal and matched tumor tissues. A short transcript with a deletion of nucleotides 154–1054 is frequently presented in late-stage breast cancers. TSG101 protein expression was also detected by Western blot analysis in 30 breast cancer patients. A predicted full-length 46 kDa and three proteins with smaller molecular weight were detected. The full-length 46 kDa protein was less expressed in tumor specimens. Immunohistochemical stains from 10 patients of each stage 0–4 revealed that TSG101 protein was predominantly present in the cytoplasm. Cell nuclei were occasionally immunopositive and the chromosomes were deeply stained during cell division. The intracellular location and the expression of TSG101 protein were both not stage-dependent in primary breast cancers. In addition, normal mammary glands were more homogenously immunopositive than invasive ductal carcinoma. These results support the notion that the aberrant expression of TSG101 in breast cancer is associated with altered cell growth.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1023/A:1006426400524

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Uncoupling of translocation across microsomal membranes from biosynthesis of influenza virus hemagglutinin (1988)

Chao, Chuck C.-K. ; Bird, Phil

New York, N.Y. : Wiley-Blackwell

Journal of Cellular Biochemistry 36 (1988), S. 289-295

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ISSN: 0730-2312

Keywords: in vitro translation ; endoplasmic reticulum ; influenza hemagglutinin ; Life and Medical Sciences ; Cell & Developmental Biology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Chemistry and Pharmacology , Medicine

Notes: This communication presents our recent studies on the biosynthesis of influenza virus hemagglutinin (HA) in a mammalian-cell-free system and its translocation across microsomal membranes. RNAs coding for wild-type (full-length) and mutant (truncated) forms of HA were generated by in vitro transcription by using bacteriophage T7 DNA-dependent RNA polymerase. These RNAs were translated in a rabbit reticulocyte system that was supplemented with dog pancreas membranes, either before translation was initiated or after it had been artificially terminated with the antibiotic cycloheximide. All forms of HA could be cotranslationally translocated. However, only truncated molecules (83% of full length) could translocate after protein synthesis had been terminated. Posttranslational translocation was dependent on the presence of a functional N-terminal signal sequence and occurred only in the presence of ribosomes. The molecular mechanism of protein targeting and translocation across the membrane of the endoplasmic reticulum is discussed based on the signal hypothesis.

Additional Material: 2 Ill.