Transgelin 2 Proteins (TAGLN2)

Mouse (Murine) Transgelin 2 (TAGLN2) interaction partners

1. dual functional nature of TAGLN2-G-actin polymerization and Arp2/3 complex inhibition-may account for the mechanisms of filopodia development at the edge of Arp2/3-rich lamellipodia in various cell types

2. These results revealed a novel function of TAGLN2 as a molecular armament required for host defense.

3. transgelin-2 may also be involved in IS stability in B-cells, thereby influencing T-cell function

4. All these results indicated a crucial role for Tagln2 in TECs for tumor development and metastasis.

5. A novel function of TAGLN2 in enhancing T cell responses by controlling actin stability at the immunological synapse.

6. The results indicate that miR-133b may play important roles in the growth and maturation of oocytes by regulating its potential target, TAGLN2, at both transcription and translation levels.

7. we demonstrate that methylation of SM22alpha promoter is an important event in vascular smooth muscle cell calcification and that high phosphate induces this epigenetic modification.

8. data demonstrate that SM22beta is a novel actin-associated protein with a unique cell lineage-restricted pattern of expression

Human Transgelin 2 (TAGLN2) interaction partners

1. dual functional nature of TAGLN2-G-actin polymerization and Arp2/3 complex inhibition-may account for the mechanisms of filopodia development at the edge of Arp2/3-rich lamellipodia in various cell types

2. TAGLN 2 overexpression in HeLa cells could inhibit cell viability, migration and invasion, and it was suggested that this may occur via upregulation of the expression levels of E cadherin and inhibitor of nuclear factor kappalightchainenhancer of activated B cells (NFkappaB) (IkappaB), and downregulation of C XC chemokine receptor type 4, matrix metalloproteinase (MMP)2, MMP9, p50 and transcription factor p65.

3. Authors found transgelin-2 expression was induced by KRAS mutation. In the case of KRAS mutation, ERK2 interacted with 29-31 amino acids of transgelin-2 and subsequently phosphorylated the S145 residue of transgelin-2.

4. Study provides important evidence that hypoxia-inducible TAGLN2 is involved in the selection of cancer cells with enhanced EMT properties to overcome the detrimental environment of cancer cells as gamma radiation.

5. Results show that Increased expression of TAGLN2 is associated with increasing tumor grade in glioma and poor patient survival. Knockdown experiments highlighted the function of TAGLN2 in promoting glioma cell invasion, the EMT phenotype, and tumor growth.

6. Our data support a novel mechanism in diabetes-associated PDAC by which transgelin-2 mediates proliferation of PDAC cells upon insulin stimulation.

7. Results suggest that TAGLN2 might regulate activation and migration of B-cells, in particular, the entry of activated B-cells into the follicle.

8. we reviewed the basic characteristics and function of Transgelin-2 and its biological role in various types of diseases in order to provide the theoretical basis for further research and new perspectives on cancer development.

9. Our data demonstrated that TAGLN2 might be an HBx induced positive host factor involved in HBV transcription and replication and HBx related liver fibrosis and tumorigenesis

10. Transgelin-2 plays functional roles in the progression of cervical squamous cell carcinoma. Suppression of Transgelin-2 may be a new strategy for the treatment of cervical squamous cell carcinoma.

11. It is a target gene of miR-1.

12. Salvianolic acid A can reverse the paclitaxel resistance and inhibit the migration and invasion abilities of human breast cancer cells by down-regulating the expression of transgelin 2.

13. Proteomics result showed TAGLN2 as the most significant overexpression in individual bladder cancer tissues and urine specimens, and thus represents a potential biomarker for noninvasive screening for bladder cancer.

14. TAGLN2 modulates hypoxia-induced apoptosis via caspase-8 apoptotic pathway. Taken together, our data demonstrated the roles of miR-133a in hypoxia-induced apoptotic and implicate its potential in cardiac dysfunctions therapy.

15. Transgelin-2, a sequence homolog of transgelin, whose role in the tumor development might be contradictory to the role of transgelin.

16. PTTG1 and TAGLN2 are highly expressed in human pancreatic cancer, and the positive expression of PTTG1 is associated with the gender of cancer patients, suggesting that it may represent a potential therapeutic target for the treatment of pancreatic cancer

17. our data propose a novel, oncogene-tumor suppressor interplay, where oncogenic PFTK1 confers HCC cell motility through inactivating the actin-binding motile suppressing function of TAGLN2 via phosphorylation.

18. Data indicate that TAGLN2 may have an oncogenic function and may be regulated by miR-1, a tumor suppressive miRNA in HNSCC.

19. in pulmonary adenocarcinoma, overexpression of TAGLN was strictly localized to the tumor-induced reactive myofibroblastic stromal tissue compartment, whereas overexpression of TAGLN2 was exclusively localized to the neoplastic glandular compartment