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Figure 6. Shows the presence of two binding sites for the D1 peptide on the NH-2 terminal region of the fibrin monomer.

Table 2 shows that the anti-proliferative effect of angiostatin is reversed by an anti-α subunit ATP antibody.

In the paragraph labeled "Low content of ATP synthase subunit ε, but increased content of subunit c is present in patient mitochondria". Figure 6 shows the patient mitochondria with accumulated Fo subunit c of ATP synthase. Figure 5 shows a mutated subunit ε is incorporated in the ATP synthase complex.

Figure 3 shows compared with patients with β cardiac myosin heavy-chain mutations, patients with cardiac troponin T mutations had a higher incidence of death before the age of 30 years. Table 3 shows each cardiac troponin T mutation produced an increase in the maximal thickness of the left ventricular wall.

Table 2.

Figure 2d shows LGMD1A muscle exhibiting patches of striking Z-line irregularity.

Figure 2 shows EC deficient in myoferlin which show defective membrane repair. Figure 3 shows that myoferlin down-regulation disrupts VEGF intracellular signaling pathways through VEGFR-2 degradation.

Figure 3C shows that Cys421Ala and Cys431Ala mutations significantly decrease the self-ubiquitination of Parkin.

Figure 1B shows that Parkin selectively interacts with UbcH8.

Figure 4C shows that ubiquitination of CDCrel-1 is significantly increased in the presence of Parkin.

Figure 4C shows that synphilin-1A promotes the death of ≈20% of the transfected neurons after 72 hours.

Figure 3

Figure 4 shows acetylation of histones by recombinant PCAF suppresses the inhibition of activated transcription by MSK1.

Figure 2 shows DNA damage causes monoubiquitylation without proteasome recruitment. Figure 3 shows UV-induced local monoubiquitylation is dependent on functional NER.

Figure 6 shows RNF8 is required for H2AX ubiquitylation following DNA damage.

Figure 6 shows the effects of FAD on the NOD activities of flavoHbs. This suggests dissociation and reassociation of bound FAD during enzyme turnover.

Figure 5 and Figure 6

Figure 4 shows the dose dependence of PDB-induced down-regulation of 80K mRNA and specificity of phorbol ester-induced down-regulation of 80K mRNA. Figure 5 shows the effect of PKC depletion on the phorbol ester-induced decrease in 80K mRNA levels and the extended time-course for PDB-induced down-regulation of 80K mRNA.