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

Leg-arista-wing complex (lawc) mutations affect the expression of D. melanogaster proteins homologous to a human basic transcription factor, TBP (TATA-box binding protein) Related Factor 2 (TRF2), specifically involved in development. The paper for the first time reports the application of genetic screens for various genomic regions to recover genetic interactions between the lawc/Trf2 gene and other genes and genetic loci by using Deficiency Kit lines with small deletions in total providing maximal coverage of the genome. The deletion mapping allowed us to recover 26 genomic regions that, when deleted, are lethal or modify the mutant phenotype due to a decreased TRF2 expression level. These deletions could be useful in identifying both novel TRF2 targets and its positive and negative regulators. There is evidence that TRF2 can be a component of high molecular DNA Replication-related Element Factor (DREF)- and Nucleosome Remodeling Factor (NURF)-containing complexes. The present study for the first time reports new genetic interactions of lawc/Trf2 with genes that encode basic and specific transcription factors. In most cases, if mutated, those genes caused developmental defects or death of progeny. However, in the case of the e(y) 1 gene, coding for the Taf9 transcription factor, only the male reproductive system is impaired when the lawc/Trf2 phenotype is associated with a e(y)l gene mutation. Mutant lawc(p1)e(y)1(u1) males become infertile due to primary spermatocyte maturation arrest and impaired premeiotic chromosome condensation in germ cells.
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PMID:[Recovery of genomic regions affecting lawc/Trf2 expression during Drosophila melanogaster development]. 2310 10

Immune responses and metabolic regulation are tightly coupled in all animals, but the underlying mechanistic connections are nowhere completely clear. In flies and in humans, prolonged or excessive immune activation can drive metabolic disruption and cause loss of metabolic stores. Conversely, disruptions of metabolic homeostasis, such as periods of malnutrition, can have significant impacts on immune function. We have recently identified the transcription factor MEF2 as a critical switch between anabolic and immune function in the adult Drosophila fat body. A conserved phosphorylation determines the affinity of MEF2 for the TATA-binding protein, effecting a choice between energy storage and immune function. The goal of this review is to place this molecular event in the broader context of metabolic-immune interaction in Drosophila, exploring what is and is not known about the ties between these 2 critical physiological functions.
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PMID:Immune-metabolic interaction in Drosophila. 2548 52