Proteins TGN46 and GP73 utilize retrograde membrane transport to maintain their predominant Golgi localization

In cells depleted of SMAP2, both proteins still localized at the Golgi, indicating that SMAP2 does not contribute to the retrograde transport of TGN46 and GP73. Thus, SMAP2 showed specificity for retrograde cargoes: SMAP2 is selectively involved in the transprot of CTxB. Whether SMAP2 is involved in retrograde transport of cellular proteins remains to be determined. The apparent no-effect on TGN46 and GP73 localization upon SMAP2 depletion highly contrasted with the effect of evection-2 depletion, where TGN46 and GP73 redistributes from the Golgi to endosomal compartments. Therefore, evection-2 requires SMAP2 for the retrograde transport of CTxB, but not that of TGN46 and GP73. Evection-2 might use a different Arf GAP to regulate the retrograde transport of TGN46 and GP73. Based on high-through genomewide transcriptome data, AbMole 11-hydroxy-sugiol molecular subtypes of human cancer have been identified and characterized by different biology. For example, distinct subtypes of breast cancer were associated with different patterns of therapeutic response, different preferential sites of relapse. In head and neck cancer, different molecular subtypes were associated with distinct patterns of copy-number alteration of canonical cancer genes. In colorectal cancer, subtypes shared similarities to distinct cell types within the normal colon crypt and shows differing degrees of ��stemness’ and Wnt signaling. A recent study depicted the molecular commonality between basal-like breast cancer and ovarian cancer by correlation analysis of transcriptional profile, but it was unclear whether the basal-like breast cancer had a ��friendship’ with any particular subtype of ovarian cancer. Actually, molecular cancer subtypes with similar biological characteristics were already found at different tissue sites. For example, both the Mes subtype of glioma and claudin-low intrinsic subtype of breast cancer were characterized by expression of mesenchymal markers and immune response. Taking together, a question was raised that whether subtypes with similar phenotype, or similar clinical outcome, would show correlation at a molecular level? To answer this question, we performed correlation analysis of transcriptional profile and pathway profile of ovarian cancer, breast cancer, hepatocellular carcinoma, glioma, lung squamous carcinoma and nasopharyngeal carcinoma. Furthermore, we analyzed pathway activities for each subtype and identified pathway frequently perturbed across different tissues. We first asked whether subtypes with similar phenotype or similar clinical outcome could be correlated by transcriptional profile and/or pathway profile. To answer this question, we measured between-subtype commonality by correlation analysis of transcriptional profile and pathway profile. A similar landscape was found for both two molecular profiles but the overall level of spearman rank correlation coefficients of pathway profiles was higher.