Polymerase I and Transcript Release Factor (PTRF) ELISA Kits

Zebrafish Polymerase I and Transcript Release Factor (PTRF) interaction partners

1. Cavin1b is essential for zebrafish notochord caveola formation, where caveolae in the notochord is required for mechanoprotection of notochord cells from mechanical stress-induced disruption and necrosis.

Human Polymerase I and Transcript Release Factor (PTRF) interaction partners

1. Overexpressing PTRF induced the malignancy of nearby cells in vivo, suggesting that PTRF alters the microenvironment through intercellular communication via exosomes in glioblastoma.

2. Data suggest that PTRF is present in the bloodstream and associates with exosomes; visceral adipose tissue may be a source of plasma PTRF; PTRF is rapidly processed inside adipocytes and promotes glucose absorption in adipocytes.

3. PTRF inhibits the proliferation, migration, and invasion of colorectal cancer cells. Future studies need to define the role of PTRF in the regulation of chemo-resistance in colorectal cancer cells and in colorectal cancer stem cells.

4. Purified Cavin1 60S complexes were analyzed structurally in solution and after liposome reconstitution by electron cryotomography. Cavin1 adopted a flexible, net-like protein mesh able to form polyhedral lattices on phosphatidylserine-containing vesicles. Mutating the two coiled-coil domains in Cavin1 revealed that they mediate distinct assembly steps during 60S complex formation.

5. Data suggest that the predominant plasmalemmal anionic lipid phosphatidylserine is essential for proper caveolin/cavin clustering, caveola formation, and caveola dynamics; membrane scrambling (by using other phospholipids) can perturb caveolar stability; these studies involved caveolin-1 and cavin-1 as models of caveolin/cavin clustering.

6. DNA methylation profiling identifies PTRF/Cavin-1 as a novel tumor suppressor in Ewing sarcoma when co-expressed with caveolin-1, which PTRF, disrupts the MDM2/p53 complex, leading to apoptosis.

7. Results show that PTRF is a direct target of miR-187. PTRF plays crucial roles in miR-187-induced epithelial-mesenchymal transition and migration of non-small cell lung cancer cells.

8. The expression of the PTRF protein was significantly weaker than that in the adjacent normal lung tissues using immunohistochemical staining. The findings revealed that miR187 promotes cell growth and invasion by targeting PTRF and miR187 may be a new prognostic factor for nonsmall cell lung cancer

9. A homozygous PTRF mutation was identified in patient-1. Congenital generalized lipodystrophy type 4 was caused by homozygous PTRF c.481-482insGTGA (p.Lys161Serfs*41) mutation in patient-2.

10. This study reports an unanticipated function of ROR1 as a scaffold of cavin-1 and caveolin-1, two essential structural components of caveolae.

11. Cavin-1 and cavin-2 are strongly expressed within caveolae-like structures within liver sinusoidal endothelial cells of the hepatitis C-related cirrhotic liver and cavin-1 would play a critical role in regulating aspects of caveolin-1.

12. Rather than forming a single coat complex containing the three cavin family members, single-molecule analysis reveals an exquisite specificity of interactions between cavin1, cavin2 and cavin3.

13. Our data support a role for PTRF/cavin-1, through caveolae formation, as an attenuator of the non-caveolar functionality of Cav1 in Gal3-Cav1 signalling and regulation of focal adhesion dynamics and cancer cell migration.

14. this study presents a novel mutation of PTRF from Saudi Arabia and our findings broaden the mutation spectrum of PTRF in the familial CGL4 phenotype.

15. cavin3 is recruited to the caveolae coat by cavin1 to interact with caveolin1 and regulate the duration time of caveolae at the plasma membrane.

16. The presence of caveolae as an anatomic structure is not sufficient to ensure their proper function in patient with PTRF mutation.

17. Using in silico and in vitro analysis we show that Cavin-1 is expressed in myogenic Rhabdomyosarcoma tumors and human and primary mouse RMS cultures. Cavin-1 or Cav-1 knockdown led to impairment of cell proliferation and migration.

18. PTRF acts as a modulator in GBM chemoresistance

19. In human adipose tissue, PTRF mRNA levels positively correlated with markers of lipolysis and cellular senescence. A negative relationship between telomere length and PTRF mRNA levels was observed in human subcutaneous fat.

20. caveolin-1 in advanced prostate cancer is present outside of caveolae, because of the lack of cavin-1 expression

Mouse (Murine) Polymerase I and Transcript Release Factor (PTRF) interaction partners

1. Data suggest that Ptrf is present in the bloodstream and associates with exosomes; visceral adipose tissue may be a source of plasma Ptrf; Ptrf is rapidly processed inside adipocytes and promotes glucose absorption in adipocytes.

2. The authors show here in mature adipocytes, ribosomal transcription can be acutely regulated in response to metabolic challenges. This acute response is mediated by PTRF (polymerase I transcription and release factor, also known as cavin-1), which has previously been shown to play a critical role in caveolae formation.

3. The current analyses reveal roles for cavin-1 and related proteins in governing myocardial contractile function and compliance, coronary and cardiac responses to mechanical and ischaemic stressors, and membrane permeability/fragility

4. acetylated cavin-1 preferentially interacted with hormone-sensitive lipase and recruited it to the caveolae, thereby promoting lipolysis.

5. these results suggested that the membrane dynamics in cell migration is affected by caveolae associated PTRF/cavin-1.

6. study demonstrates a critical role of cavin-1 in vascular structure and function, but the influences on arterial resistance cancel each other such that arterial blood pressure remains unaltered in homeostatic conditions

7. lipid mobilization in cultured adipocytes to induce lipid droplet shrinkage led to biphasic response of cavin-1 with ultimate loss of expression of cavin-1 by protein degradation.

8. A Western-type diet in apo-E2 knock-in mice produced 3 groups of obese mice with PTRF expression correlating with glucose tolerance: normal, hyperinsulinemic glucose-tolerant, or impaired. PTRF compromised adipocyte differentiation of 3T3-L1 cells.

9. Adipocytes from cavin-1-null mice are markedly dysfunctional exhibiting decreased insulin-dependent glucose uptake, fatty acid uptake, and lipolysis.

10. PTRF is a crucial regulator of TLR4 signaling in the development of sepsis.

11. an important role for Cavin1 in lung homeostasis

12. Cavin-1 is critical for detrusor caveolae and for overall contractility and structure of the urinary bladder.

13. Cavin-1 modulates cellular polarization, and the subcellular localization of Rac1 and caveolin-1 in migrating cells as well as PKCalpha caveola recruitment.

14. Double-immunogold labeling showed that the caveolae-shaping molecule PTRF/cavin 1 behaved similarly and that syndapin II and PTRF/cavin 1 colocalized.

15. membrane-delimited interaction between MG53 and PTRF contributes to initiation of cell membrane repair

16. Our study is the first direct demonstration for a novel adipose tissue-specific function of PTRF as a mediator of lipolysis and also shows that phosphorylation of PTRF is required for efficient fat mobilization.

17. We conclude that PTRF-Cavin is required for caveola formation and sequestration of mobile caveolin into immobile caveolae.