Disease relevance of TOB1

• Using RT-PCR and immunohistochemical staining of tissue microarrays, we could reveal a differential mRNA and protein expression of TOB1 in the majority of breast tumors and lymph node metastases compared with normal breast tissues, indicating a potential role of this protein in breast tumorigenesis [1].
• Tob1 expression was also detected at a decreased level in isolated chondrocytes and in the chondrosarcoma cell line HCS-2/8 [2].

High impact information on TOB1

• Tob55 is part of the hetero-oligomeric TOB (topogenesis of mitochondrial outer-membrane beta-barrel proteins) or SAM (sorting and assembly of mitochondria) complex, which is present in the mitochondrial outer membrane [3].
• We have investigated the biogenesis of the TOB complex [4].
• Of these genes, TOB1 (transducer of ERBB2) was selected for further expression analysis [1].
• This gene is homologous to the human BTG1, BTG2 and TOB genes which were demonstrated to act as inhibitors of cell proliferation [5].
• The BTG4 gene, encoding BTG/TOB family protein, as well as the SIK2 gene, encoding salt-inducible serine/threonine kinase 2, were also located within the 11q23.1 region [6].

Biological context of TOB1

• RESULT(S): Array analyses revealed a cell-cycle regulatory gene, Tob-1, which was differentially expressed by the two cell types after incubation with IL-1beta [7].
• Altered expression of a cell-cycle suppressor gene, Tob-1, in endometriotic cells by cDNA array analyses [7].
• Altogether, the downregulation of the expression of Tob1 in osteoarthritic chondrocytes might be an important aspect of the cellular processes taking place during osteoarthritic cartilage degeneration [2].
• Activation, the reinitiation of proliferative activity and the loss of a stable phenotype are three major changes in osteoarthritic chondrocytes that are highly significantly correlated with the repression of Tob1 expression [2].

Anatomical context of TOB1

• Replicate Northern analyses (n = 4) showed that exposure to IL-1beta for 12 hours resulted in a 25% +/- 5% diminution of Tob-1 mRNA in endometriotic stromal cells [7].
• Seventy-four patients received 250 units (3.3 units/pt) of Group O red blood cells (TOB), and nine patients received 27 units of type-specific blood (TSB) (3.0 units/pt) [8].
• In addition, the ceramic material was osteoconductive and animals in TCPL + TOB and TCPL carrier alone showed evidence of osteoblast alkaline phosphatase activity for a period of 15 weeks [9].

Associations of TOB1 with chemical compounds

• On consecutive mornings the patients were given either tobramycin intravenously (i.v.) over 3-5 min (TOB phase), or tobramycin i.v. over 3-5 min followed immediately by ticarcillin infused i.v. over 20-30 min (TOB+TIC phase) [10].

Analytical, diagnostic and therapeutic context of TOB1

• To study the safety of TOB used as an immediate resuscitation component, a 30-month prospective study of all patients arriving at a single trauma unit was undertaken [11].
• Northern blotting and subsequent quantitative densitometric evaluation was done to confirm steady-state levels of Tob-1 mRNA transcripts [7].
• The repression of Tob1 was confirmed by quantitative PCR and correlated to markers of chondrocyte activity and proliferation in vivo [2].

References