Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20226 (TATA-binding protein)
 1,297 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

p53 is a nuclear protein that acts like a tumor suppressor and is involved in regulation of cellular growth. In Xenopus, the p53 protein is highly expressed during oogenesis and is strictly cytoplasmic in the oocyte. We have analysed its participation in DNA replication and transcription during early development, using the egg and oocyte as model-systems. The injection of sperm nuclei into Xenopus eggs is followed by DNA replication and mitotic events. We show that the endogenous p53 enters the nuclei and moves through a series of discrete sub-nuclear loci whose distribution is S-phase specific. A specific peripheral nuclear localization of p53 is observed before entry into S-phase, followed by an internal localization which is strictly dependent on ongoing DNA synthesis. At no stage in the cell cycle, however, did we observe any co-localization with RPA or PCNA, which were used as initiation or elongation markers for DNA replication. We also show that injection into the nucleus of the oocyte of small amounts of either Xenopus or human p53 - less than 10% of the cytoplasmic storage - is sufficient to block RNA polymerase II-dependent transcription from a coinjected TATA-box-containing reporter plasmid. Transcription is rescued by microinjection of the TATA-box binding protein (TBP), suggesting that nuclear exclusion of p53 during oogenesis may be necessary for transcription of maternal genes. These characteristics are discussed in relation to the regulation of nuclear activities during early embryogenesis.
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PMID:A functional analysis of p53 during early development of Xenopus laevis. 939 77

TBP (TATA-binding protein)-related factor 2 (TRF2) regulates transcription during a nuber of cellular processes. We previously demonstrated that it is localized in the cytoplasm and is translocated to the nucleus by DNA-damaging agents. However, the cytoplasmic localization of TRF2 is controversial. In this study, we reconfirmed its cytoplasmic localization in various ways and examined its nuclear migration. Stresses such as heat shock, redox agents, heavy metals, and osmotic shock did not affect localization whereas genotoxins such as methyl methanesulfonate (MMS), cisplatin, etoposide, and hydroxyurea caused it to migrate to the nucleus. Adriamycin, mitomycin C and gamma-rays had no obvious effect. We determined optimal conditions for the nuclear migration. The proportions of cells with nuclei enriched for TRF2 were 25-60% and 5-10% for stressed cells and control cells, respectively. Nuclear translocation was observed after 1 h, 4 h and 12 h for cisplatin, etoposide and MMS and hydroxyurea, respectively. The association of TRF2 with the chromatin and promoter region of the proliferating cell nuclear antigen (PCNA) gene, a putative target of TRF2, was increased by MMS treatment. Thus TRF2 may be involved in genotoxin-induced transcriptional regulation.
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PMID:TATA-binding protein-related factor 2 is localized in the cytoplasm of mammalian cells and much of it migrates to the nucleus in response to genotoxic agents. 1708 73

Transcription factor IID (TFIID), as a general transcription factor, plays a pivotal role in the preinitiation complex (PIC) assembly and transcription initiation by recruiting RNA polymerase II to the promoter. The TFIID complex contains the TATA-box binding protein (TBP) and a group of conserved TAF proteins. However, its distribution and function in the central nervous system (CNS) are more diverse than previously understood. Here, we mainly investigated the spatiotemporal expression and cellular localization of TBP/TFIID during spinal cord injury (SCI) in adult rats. Western blot analysis revealed that TBP/TFIID was present in normal rat's spinal cord. It gradually increased, reached a peak at the third day after SCI, and then decreased. We observed that TBP/TFIID was widely distributed in spinal cord, mainly in neurons and glial cells. In addition, Western blot detection also showed that the third day post-injury was the proliferation peak indicated by the elevated expression of proliferating cell nuclear antigen (PCNA), a marker of proliferating cells. Importantly, injury-induced expression of TBP/TFIID was colabelled by PCNA showed the increase of TBP/TFIID expression in proliferating astrocytes and microglia. Collectively, we hypothesize that TBP/TFIID may be implicated in the proliferation of astrocytes and microglia and the recovery of neurological outcomes.
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PMID:Increased Expression of TBP/TFIID after spinal cord injury in adult rats. 2471 Aug 3