Disease relevance of BCLAF1

• Emerin binding to Btf, a death-promoting transcriptional repressor, is disrupted by a missense mutation that causes Emery-Dreifuss muscular dystrophy [1].
• It has been suggested that a well-planned neurointensive care management can effectively reduce the secondary brain insults.The BTF and the AANS proposed the Guidelines for the Management of Severe Head Injury in 1995 [2].

High impact information on BCLAF1

• Indeed, the sustained overexpression of Btf in HeLa cells induced apoptosis, which was inhibited by E1B 19K [3].
• Expression of Btf also inhibited transformation by E1A with either E1B 19K or mutant p53, suggesting a role in either promotion of apoptosis or cell cycle arrest [3].
• BTF includes new methods for describing past ecosystems, designing fisheries that meet criteria for sustainability and responsibility, and evaluating the costs and benefits of fisheries in restored ecosystems [4].
• Quantum mechanical calculations and X-ray crystallographic studies of this ensemble of reactions by BTF, and the analogous set of reactions by its progenitor, tetracyanoethylene (TCNE), reveal several interesting facets [5].
• Reaction of 2,2-bis(trifluoromethyl)-1,1-dicyanoethylene (BTF; 1) with 6,6-dimethylfulvene (2) affords the expected Diels-Alder cycloadduct, 7-(1-methylethylidene)-3,3-bis(trifluoromethyl)bicyclo[2.2.1]hept-5-ene-2,2-dicarbonitrile (3), in good yield [5].

Anatomical context of BCLAF1

• In a yeast two-hybrid screen, we found that emerin interacts with Btf, a death-promoting transcriptional repressor, which is expressed at high levels in skeletal muscle [1].
• However, within 3 h after treating cells with Fas antibody to induce apoptosis, the distribution of Btf changed, and Btf concentrated in a distinct zone near the nuclear envelope [1].
• The control, known as ColorSeed C&G (BTF Pty Ltd, Sydney, Australia), is a suspension containing exactly 100 Cryptosporidium oocysts and 100 Giardia cysts that have been modified by attachment of Texas Red to the cell wall, allowing them to be differentiated from unmodified oocysts and cysts [6].

Associations of BCLAF1 with chemical compounds

• Using a collection of 21 clustered alanine-substitution mutations in emerin, the residues required for binding to Btf mapped to two regions of emerin that flank its lamin-binding domain [1].
• Finally, an explanation is offered for the preference of the persubstituted cyanoolefins BTF and TCNE to add to the exocyclic diene portion of 1-isopropenyl-1,3-cyclopentadiene and the contrasting preference of 2-acetyloxy-2-propenenitrile to add to the endocyclic diene [5].
• The conversion of 3 to 8 proceeds by the initial retro-Diels-Alder reaction followed by isomerization of the fulvene to 1-isopropenyl-1,3-cyclopentadiene that then reacts with BTF to give the alternative Diels-Alder product as a single regioisomer [5].
• CONCLUSION: We identified a transcriptional repressor of survival genes, known as BTF, which triggers a proapoptotic signal, potentially helpful to overcome the resistance to STI571 [7].

Physical interactions of BCLAF1

• Biochemical analysis showed that emerin binds Btf with an equilibrium affinity (KD) of 100 nm [1].

Other interactions of BCLAF1

• Two disease-causing mutations in emerin, S54F and Delta95-99, disrupted binding to Btf [1].

Analytical, diagnostic and therapeutic context of BCLAF1

• Bladder tumor fibronectin (BTF; ng/ml) was determined by solid phase, two-site chemiluminescent immunometric commercial diagnostic assay developed for the Immulite automated immunoassay system (Diagnostic Products Corporation, Los Angeles, CA, USA) [8].

References