High impact information on TBCD

• Tubulin folding cofactor D is a microtubule destabilizing protein [1].
• Downregulation of tfcD mRNA expression by shear stress was defined at the level of transcription by nuclear run-on assays [2].
• The encoded amino acid sequence of the human endothelial SSD-1 isoform (4.1-kb mRNA species) revealed 80.4% identity and 90.9% homology to the bovine ss-tubulin folding cofactor D (tfcD) gene [2].
• The shear stress-dependent downregulation of tfcD mRNA and protein was attenuated by the NO synthase inhibitor Nomega-nitro-L-arginine methyl ester [2].
• Using the method of RNA arbitrarily primed polymerase chain reaction, we cloned a polymerase chain reaction fragment representing an mRNA species downregulated by arterial compared with venous shear stress (shear stress downregulated gene-1, SSD-1) [2].

Biological context of TBCD

• Single copy expression of SSD1/SRK1 was sufficient to suppress the thermosensitive phenotype, and high copy expression partially suppressed the splicing and U4/U6.U5 tri-snRNP assembly pheno-types [3].

Anatomical context of TBCD

• Because tfcD was shown to be a microtubule-destabilizing protein, our data suggest a shear stress-dependent regulation of the microtubular dynamics in human endothelial cells [2].

Analytical, diagnostic and therapeutic context of TBCD

• According to Northern blot analysis, corresponding SSD-1 cDNA clones revealed a similar, time-dependent downregulation after 24 hours of arterial shear stress compared with venous shear stress or static controls [2].

References