anti-Tumor Susceptibility Gene 101 (TSG101) Antibodies

Fruit Fly (Drosophila melanogaster) Tumor Susceptibility Gene 101 (TSG101) interaction partners

1. loss of ept alters nuclear cell cycle control in developing imaginal discs and the DaPKC, presenilin, and rbf1 genes as modifiers of molecular and cellular phenotypes that result from loss of ept

2. analysis of genetic interactions between the Drosophila tumor suppressor gene ept and the stat92E transcription factor

Human Tumor Susceptibility Gene 101 (TSG101) interaction partners

1. By increasing the stability of the TSG101 protein, TSG101154-1054 specifically enhanced TSG101-mediated TW01 cell migration and invasion, suggesting the involvement in NPC metastasis in vivo. This finding sheds light on the functional significance of TSG101154-1054 generation via re-splicing of TSG101 mRNA in NPC metastasis.

2. TSG101 promotes proliferation of renal cell carcinoma cells

3. identification of HIV-1 Gag-TSG101 interaction inhibitors.

4. this is the first study that implicates the importance of TSG101 in anoikis resistance of thyroid cancer.

5. In LNCaP prostate cancer cells, TSG101 overexpression recruits the androgen receptor (AR) to TSG101-containing cytoplasmic vesicles resulting in reduced AR protein level and AR transactivation activity downregulation. Immunofluorescence microscopy demonstrated that TSG101-decorated cytoplasmic vesicles are associated with late endosomes/lysosomes.

6. The authors provide evidence that the ubiquitin (Ub) E2 variant domain of Tsg101 provides chaperone function to HIV-1 Gag that is independent of its interaction with the Pro-Thr-Ala-Pro motif, supporting the hypothesis that the domain provides a function in addition to its well-established role in cellular endosomal sorting complex required for transport factor recruitment.

7. In this review, HIV-infected cells have TSG101 on their surface and thus can be used in antibody-based therapies. The development of a monoclonal antibody CB8-2 lessens the assembly of viruses from infected cells

8. Results indicate that Vpr overcomes the effects of TSG101 overexpression to support viral production by competing with TSG101 to bind Gag.

9. our studies reveal that Tsg101 plays a role in the trafficking of macropinocytosed Kaposi's sarcoma-associated herpesvirus in the endothelial cells

10. Knockdown of LAMP2A, a CMA-related protein, and TSG101, an mA-related protein, significantly but only partially decreased the punctate accumulation of GAPDH-HT in AD293 cells and primary cultured rat cortical neurons.

11. the variant alleles of TSG101 rs2292179 and ATF2 rs3845744 were associated with a reduced risk of breast cancer, particularly for subjects with BMI <24 (kg/m(2)) and postmenopausal women, respectively

12. TSGDelta154-1054 splice variant increases TSG101 oncogenicity by inhibiting its E3-ligase-mediated proteasomal degradation.

13. Results show that TSG101 bidirectionally modulates cell invasion through regulating MMP-9 mRNA expression in different cell types.

14. TSG101 plays an important role in the development of hepatocellular carcinoma

15. Expression of tsg101 mRNA and of TSG101 protein were significantly higher in the oxaliplatin resistant cell line than parent HT-29 cels.

16. PSAP motif of OFR3 is required for hepatitis E virus exit and interaction with host TSG101.

17. Stress-internalized EGFR is retained intracellularly by continued p38 activity in a mechanism involving ubiquitin-independent, ESCRT/ALIX-dependent incorporation onto intraluminal vesicles (ILVs) of MVBs

18. Tsg101 is necessary for the efficient transport and release of nucleocapsids in marburg virus-infected cells

19. our findings strongly suggest that TSG101 is a cellular target for HSV-1 tegument ubiquitin specific protease activity during infection.

20. Our findings thus indicate that TSG101 regulation of p21 is an important factor in the cellular function of TSG101.

Mouse (Murine) Tumor Susceptibility Gene 101 (TSG101) interaction partners

1. mechanical stress upregulates TSG101 in podocytes.

2. Tsg101 was deleted from mature oligodendroglia in vivo. This resulted in severe spongiform encephalopathy, histopathologically similar to that observed in Mgrn1 null mutant mice but with a more rapid onset.

3. BLOS1 interacts with sorting nexin 2 and the ESCRT-I component TSG101 to mediate the sorting of EGFR into endosomal compartments

4. pigment-type switching likely requires MGRN1's ubiquitin ligase activity but not its ability to bind TSG101 or NEDD4.

5. Tsg101 has a role in expression of EGFR and ErbB2 and preventing induction of autophagy prior to cell death

6. show that ubiquitin recognition by TSG101 is required for cSMAC formation, T cell receptor (TCR) microcluster signal termination, TCR downregulation.

7. Negative regulation of cell growth and differentiation by TSG101 through association with p21(Cip1/WAF1).

8. Targeted deletion results in cell cycle arrest and p53-independent cell death

9. our results suggest that Tsg101 is required for normal cell function of embryonic and adult tissues but that this gene is not a tumor suppressor for sporadic forms of breast cancer.

10. the TSG101 interaction with HRS is a crucial step in endocytic down-regulation of mitogenic signaling and this interaction may have a role in linking the functions of early and late endosomes

11. the important role for cell survival

12. the Tsg101 protein has only weak oncogenic properties

13. results suggest that TSG101 is involved in the degradation of connexins via interaction with connexin proteins

14. Loss of MGRN1 promotes ubiquitination of TSG101 by other ubiquitin ligase E3s and may prevent its disassociation from endosomal membranes or cause it to form insoluble aggregates.