anti-Pituitary Tumor-Transforming 1 (PTTG1) Anticorps

Human Pituitary Tumor-Transforming 1 (PTTG1) interaction partners

1. PTTG and PBF interact in head and neck squamous cell carcinoma to reduce p53 stability and function

2. Higher levels of PTTG1 were observed in hepatocellular carcinoma (HCC) tumor tissues. Its expression is regulated by PTTG3P in HCC.

3. Cancer-associated fibroblasts (CAFs) could induce pituitary tumor transforming gene (PTTG) over-expression and increase endometrial cancer (EC) cell invasion and migration in vitro.

4. We found that PTTG overexpression in pituitary tumor cells is explained by its protein stabilization, is regulated by RSUME and accounts for PTTG tumor abundance and pathogenic action. There is no evidence so far that this mechanism operates in normal cells. This finding puts in a central role the protein stabilization-overexpression of proto-oncogenes as major regulators of cellular dysfunction.

5. High PTTG1 expression was associated with Adrenocortical Carcinoma.

6. the short form of securin does not influence the expression of MYC transcriptional targets, such as TP53 and IL-8.

7. Data strongly indicated that PTTG1 is a target gene of miR186 in osteosarcoma (OS) cells and is involved in miR186mediated suppressive effects of OS cells.

8. Results show that PTTG1 oncoprotein overexpression may modulate cell proliferation-related regulators in myeloid leukemia.

9. In ACTH-secreting pituitary tumors, IHC staining showed strong cytoplasmic and moderate nucleic PTTG immunoreactivity in 22 of 28 nonrecurrent tumors and in 21 of 27 recurrent tumors but no staining in the 2 normal pituitaries. PTTG was significantly increased in both the nonrecurrent and recurrent groups compared with normal pituitary glands, but there was no difference between the nonrecurrent and recurrent groups.

10. Smurf1 interacts with and targets Securin, an inhibitor of sister-chromatid separation, for poly-ubiquitination and proteasomal degradation.

11. PTTG-1 oexpression in meningiomas were correlated with tumor grade and proliferation rate.

12. Results found that PTTG1 expression was significantly increased in androgen-independent prostate cancer cells and, elucidates that interleukin-6/STAT3 activation can increase PTTG1 expression and, consequently, promote the resistance to androgen deprivation therapy in castration-resistant prostate cancer by inducing EMT and increasing the cancer stem cell population.

13. we confirmed the oncogenic function of PTTG1 in BC and demonstrated that PTTG1 is a target of miR-146a-3p.

14. PTTG1 is an independent prognostic factor and acts as an oncogene in colorectal cancer

15. High PTTG1 expression is associated with aggressive meningiomas.

16. These results indicate PTTG1 may be a valuable biomarker in ovarian cancer to predict sensitivity to saracatinib, and could form the basis of a targeted prospective saracatinib trial for ovarian cancer.

17. A relatively stable genome in retinoblastoma tumor cells is maintained by TRb1 and TRb2-mediated PTTG1 inhibition, counteracting Rb-deficiency-related genomic instability.

18. Findings indicate that PBF and PTTG have a critical role in promoting thyroid cancer that is predictive of poorer patient outcome.

19. PTTG-mediated FGF2 upregulation is associated with more aggressive tumor features in patients with acromegaly. Also, locally produced estrogen through aromatization might have a role in this phenomenon.

20. All these suggest that the MAP3K M1P site is a potential interacting partner of MAP3K SH3 domain, which may mediate the intermolecular recognition between hPTTG1 and MAP3K.

Pig (Porcine) Pituitary Tumor-Transforming 1 (PTTG1) interaction partners

1. PTTG1 is a new candidate maternal effect gene that may participate in the processes of oocyte maturation and zygotic genome activation during embryogenesis

Mouse (Murine) Pituitary Tumor-Transforming 1 (PTTG1) interaction partners

1. The findings show that maternal aging compromises the oocyte SAC-APC/C axis leading to a decrease in securin that ultimately causes sister chromatid cohesion loss.

2. Smurf1 interacts with and targets Securin, an inhibitor of sister-chromatid separation, for poly-ubiquitination and proteasomal degradation.

3. High PTTG1 expression is associated with pituitary tumor development.

4. PTTG is functionally required for hepatic fibrosis progression in an animal model of chronic liver injury, and thus a potential treatment target.

5. RasGrf1 is an important upstream component of signal transduction pathways regulating Pttg1 expression and controlling beta cell development and physiological responses.

6. these results implicate Pttg1 in the regulation of homotypic spacing between specific types of retinal neurons.

7. Pttg1/securin has roles in branching morphogenesis of the mammary gland and suppression of mammary tumorigenesis

8. PBF is the first protein to interact with the critical TH transporter MCT8 and modulate its function in vivo

9. CSN3 and CSN5 are involved in oocyte meiosis by regulating degradation of Cyclin B1 and Securin via APC/C.

10. The genetically deleting Tff3 in mice altered down-regulated Pttg1 and up-regulated serpina3n expression, indicating a potential role of these factors during the development of presbyacusis.

11. data reveal that up to 9 months of age, Pttg1(-/-) retinas have a healthy morphology and normal photoreceptor function

12. Pituitary tumor transforming gene 1 (PTTG1), an oncogene, was the most up-regulated transcript in KLF6+/- liver. PTTG1 downregulation represents a novel tumor suppressor pathway of KLF6.

13. Pituitary tumor transforming gene-null male mice exhibit impaired pancreatic beta cell proliferation and diabetes.

14. homologue disjunction in mouse oocytes is dependent on proteolysis of the separase inhibitor securin and cyclin B1

15. Physiological functions of PTTG are revealed by PTTG-null mice who exhibit a variety of cell growth abnormalities including diabetes mellitus secondary to defective beta-cell proliferation. Review.

16. Securin phosphorylation act redundantly to prevent sister chromatid separation.

17. results suggest that Rae1 and Nup98 are temporal regulators of APC(Cdh1) that maintain euploidy by preventing unscheduled degradation of securin

18. results suggest that the proteolysis of securin is dependent on ubiquitin-proteasome pathway and is necessary for the degradation of Rec8 during meiotic metaphase-to-anaphase transitions in oocytes

19. PTTG1 and its binding protein PTTG binding factor are expressed in pituitary FS TtT/GF cells.

20. PTTG1, an oncogene, is regulated by the liganded thyroid hormone receptor beta