The Fanconi anemia group C gene product modulates apoptotic responses to tumor necrosis factor-α and Fas ligand but does not suppress expression of receptors.

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The Fanconi anemia group C gene product modulates apoptotic responses to tumor necrosis factor-α and Fas ligand but does not suppress expression of receptors of the tumor necrosis factor receptor superfamily Paul S Koh, Grant C Hughes, Gregory R Faulkner, Winifred W Keeble, Grover C Bagby Experimental Hematology Volume 27, Issue 1, Pages 1-8 (January 1999) DOI: 10.1016/S0301-472X(98)00064-2

Figure 1 The Fanconi anemia group C (FAC) gene product does not influence tumor necrosis factor receptor (TNFR) superfamily mRNA levels. Reverse transcriptase PCR analysis of constitutive mRNA levels of TNFR1, Fas, CD30, CD40, and nerve growth factor receptor (NGFR) in isogenic human cell lines is shown. Constitutive IFNRα mRNA levels also were measured and are shown in the last set of lanes. The four lanes for each amplimer represent, from left to right, the cell lines HSC536, HSC536/neo, HSC536/FAC/neo, and JY Experimental Hematology 1999 27, 1-8DOI: (10.1016/S0301-472X(98)00064-2)

Figure 2 FAC-deficient cells constitutively express normal levels of TNFR superfamily proteins. Flow cytometric quantification of TNFR2, Fas, CD30, CD40, and NGFR in the isogenic cell lines PD149L, PD149/neo, PD149/FAC/neo, and JY is shown. Fluorescence intensity is scaled logarithmically. Solid line histograms represent receptor expression. Adjacent dotted line histograms represent respective isotypic controls Experimental Hematology 1999 27, 1-8DOI: (10.1016/S0301-472X(98)00064-2)

Figure 3 Constitutive expression of TNFR superfamily proteins is similar in FAC −/− versus FAC −/+ murine hematopoietic progenitor cells. Flow cytometric measurement of TNFR1, Fas, CD30, and CD40 surface expression by c-kit+ murine bone marrow cells is shown. Fluorescence intensity is scaled logarithmically. Solid line histograms represent receptor expression. Adjacent dotted line histograms represent respective isotypic controls. FACKO = nullizygous (FAC knockout) cells; WT = heterozygous cells Experimental Hematology 1999 27, 1-8DOI: (10.1016/S0301-472X(98)00064-2)

Figure 4 IFN-γ–induced expression of TNFR superfamily proteins is similar in FAC −/− and FAC −/+ murine hematopoietic progenitor cells. Bone marrow cells were exposed to murine IFN-γ (100 U/mL) for 12 hours and then analyzed by flow cytometry for TNFR1, Fas, CD30, and CD40 expression by c-kit+ cells. Parallel cultures without IFN-γ were used as controls and are represented by the first four histograms in each set. Fluorescence intensity is scaled logarithmically. Solid line histograms represent receptor expression. Adjacent dotted line histograms represent respective isotypic controls. FACKO = nullizygous (FAC knockout) cells; WT = heterozygous cells Experimental Hematology 1999 27, 1-8DOI: (10.1016/S0301-472X(98)00064-2)