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Consensus statement on the pathology of IgG4-related disease

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BiFC assays revealed that K-Hcy-modified HMGB1/2 disrupted SLIT2-ROBO4 interactions, as evidenced by reduced BiFC signals upon recombinant K-Hcy-HMGB1/2 treatment in 293T cells co-expressing VN155(I152L)-SLIT2-N and VC155-ROBO4 (Figure 6H-I)

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