Rabbit Anti-Human FUT4 (C-terminal) Polyclonal antibody

Objective: To investigate whether Lewis Y (LeY) carried by integrin alpha v beta 3 influences integrin alpha v beta 3-mediated adhesion in an in vitro implantation model. Design: Laboratory research. Setting: Reproduction and glycobiology research laboratory. Intervention(s): Specific antibody blockage of LeY or integrin alpha v beta 3 and knockdown of FUT4 expression in RL95-2 cells by transient transfection of FUT4 siRNA. Main Outcome Measure(s): The expression of integrin alpha v beta 3 and LeY in both endometrial tissues and RL95-2 cells was measured. LeY carried by integrin alpha v beta 3 was identified by examining the immunoprecipitated integrin alpha v beta 3. The effect of knocking down FUT4 on the expression of integrin alpha v beta 3 and LeY and their impact on the adhesion of JAR cells to the RL95-2 cells were assessed. Result(s): Integrin alpha v beta 3 and LeY are expressed in both secretory-stage human endometrial tissue and in RL95-2 cells. Although integrin alpha v beta 3 carries LeY, knocking down FUT4 expression only reduces the expression of LeY but not of integrin alpha v beta 3. Knocking down FUT4, antibody blockade of LeY or integrin alpha v beta 3 consistently decreases the adhesion of JAR cells to the RL95-2 cells and prevents focal adhesion kinase (FAK) phosphorylation. Conclusion(s): LeY carried by integrin alpha v beta 3 plays a critical role on the attachment of JAR cells to the RL95-2 cells and activates integrin alpha v beta 3/FAK signaling. (Fertil Steril (R) 2011;95:1446-51. (C)2011 by American Society for Reproductive Medicine.)

We report that the overexpression of mitochondrial ribosomal protein MRPS18-2 (S18-2) can immortalize primary rat embryonic fibroblasts (REFs). The immortalized cells (18IM) lose contact inhibition, form foci, and are capable of anchorage-independent growth. Concurrently, mesodermal markers, such as vimentin, smooth muscle actin, and Fut4, disappear completely. 18IM cells express embryonic stem cell markers, such as SSEA-1, Sox2, and Oct3/4. In confluent cultures, a portion of cells also express ectodermand endoderm-specific pan-keratin, ectoderm-specific beta-III-tubulin, mesoderm-specific MHC class II, and become stainable for fat with Oil red O. None of these changes was detected in c-myc+Ha-ras (MR)-transformed cells. In immunodeficient mice, 18IM cells formed small transiently growing tumors that have down-regulated SSEA-1 and showed pan-keratin staining. We conclude that S18-2 can immortalize REFs and induces them to express stem cell traits.