Target Alteration Quiz

Addition of **hSlit2** up to a final **concentration** of 1 microg/ml had no detectable effect on the formation of nephrons or on branching morphogenesis of the ureteric tree after 2 or 4 days in culture, as assessed via immunofluorescence for the markers WT1 and calbindin 28K respectively.

Furthermore, **expression** of **SLIT2** was restored in relatively low-expressing cell lines after treatment with 5-aza-2-deoxycytidine (5-Aza-dC).

A binding ELISA experiment in mouse bone marrow-derived macrophages showed that ROBO1, rather than ROBO3, was directly associated with SLIT2, and gene silencing with Robo1 siRNA **blocked** the **SLIT2**-mediated suppression of osteoclastogenesis.

**Overexpression** of orthodenticle homeobox 2 using lentivirus increased levels of known A10 elevated genes, including neuropilin 1, neuropilin 2, **slit2** and adenylyl cyclase-activating peptide in both MN9D cells and ventral mesencephalic cultures, whereas knockdown of endogenous orthodenticle homeobox 2 levels via short hairpin RNA reduced expression of these genes in ventral mesencephalic cultures.

**Signal transducer and activator of transcription-6** (STAT6) inhibition **suppresses** renal cyst growth in polycystic kidney disease.

**Wild-type** (WT), **Stat6** knockout (Stat6-/-), and intestinal epithelial cell-specific IL-4Rα knockout (Il-4rαΔIEC) mice were subjected to colitis-associated (AOM/DSS) and colitis-independent (sporadic) carcinogenesis.

This innate collaboration was absent in IL-4(-/-) and **signal transducer and activator of transcription (STAT)-6** **(-/-)** mice and was inhibited by anti-IL-4 treatment.

Disruption of the IL-4 signaling through either IL-4 neutralizing **antibody** or knockout of **signal transducer and activator of transcription (STAT)6** reversed the miR-17-92 cluster suppression in Th2 cells.

To study the role of Slit in early embryos, we **overexpressed** Slit2 in the whole embryos either by injection of its mRNA into one-cell stage embryos or by heat-shock treatment of the transgenic embryos which carries the **slit2** gene under control of the heat-shock promoter.

This is based on the observation that, although both Slit1 and **Slit2** are **expressed** around the ventral midline, mice defective in either gene alone exhibit few or no axon guidance defects at the optic chiasm whereas embryos lacking both Slit1 and Slit2 develop a large additional chiasm anterior to the chiasm's normal position.

Identification of single-nucleotide and repeat **polymorphisms** in two candidate genes, interleukin 4 receptor (IL4RA) and **signal transducer and activator of transcription protein 6 (STAT6)**, for Th2-mediated diseases.

**Inhibitory** Effect of **Slit2-N** on VEGF165-induced proliferation of vascular endothelia via Slit2-N-Robo4-Akt pathway in choroidal neovascularization.

Using analysis of **knock-out** mice and in vitro assays, we found that, in the mammalian retina, Slit1 and **Slit2**, known chemorepellents for RGC axons, regulate distinct aspects of intraretinal pathfinding in different regions of the retina.

Elevated temperature had no significant effect on the **level** of transcription of **these genes**.

Antibody-**drug** conjugates that target **TROP2** represent a promising approach for the treatment of TROP2-expressing cancers including lung cancer and breast cancer.

Our data demonstrate that Tacstd2 expression and membrane localization are tightly associated with stratified epithelial homeostasis, while **loss of** **TACSTD2** was identified in poorly differentiated SCC tissues collected from cervix, esophagus, head and neck.

Soluble **human leukocyte antigen-g** and its insertion/deletion **polymorphism** in papillary thyroid carcinoma: novel potential biomarkers of disease?

**Histocompatibility leukocyte antigen-G** is not **expressed** by endometriosis or endometrial tissue.

We demonstrate that **HLA-G5** **downregulates** EPOR constitutive signaling of JAK2 V617F-expressing HEL cells, leading to inhibition of cell proliferation through G1 cell cycle arrest.

Soluble **human leukocyte antigen-G** serum levels in patients with acquired immune **deficiency** syndrome affected by different disease-defining conditions before and after antiretroviral treatment.