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PTRF encodes a protein that enables the dissociation of paused ternary polymerase I transcription complexes from the 3' end of pre-rRNA transcripts.
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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.
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.
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 (show CAV1 ELISA Kits) and cavin-1 as models of caveolin/cavin clustering.
DNA methylation profiling identifies PTRF/Cavin-1 as a novel tumor suppressor in Ewing sarcoma when co-expressed with caveolin-1 (show CAV1 ELISA Kits), which PTRF, disrupts the MDM2 (show MDM2 ELISA Kits)/p53 (show TP53 ELISA Kits) complex, leading to apoptosis.
Results show that PTRF is a direct target of miR (show MLXIP ELISA Kits)-187. PTRF plays crucial roles in miR (show MLXIP ELISA Kits)-187-induced epithelial-mesenchymal transition and migration of non-small cell lung cancer cells.
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
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.
This study reports an unanticipated function of ROR1 (show ROR1 ELISA Kits) as a scaffold of cavin-1 and caveolin-1 (show CAV1 ELISA Kits), two essential structural components of caveolae.
Cavin-1 and cavin-2 (show SDPR ELISA Kits) 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 (show CAV1 ELISA Kits).
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 (show SDPR ELISA Kits) and cavin3 (show PRKCDBP ELISA Kits).
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.
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
acetylated cavin-1 preferentially interacted with hormone-sensitive lipase (show LIPE ELISA Kits) and recruited it to the caveolae, thereby promoting lipolysis.
these results suggested that the membrane dynamics in cell migration is affected by caveolae associated PTRF/cavin-1.
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
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.
A Western-type diet in apo (show C9orf3 ELISA Kits)-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.
Adipocytes from cavin-1-null mice are markedly dysfunctional exhibiting decreased insulin (show INS ELISA Kits)-dependent glucose uptake, fatty acid uptake, and lipolysis.
PTRF is a crucial regulator of TLR4 (show TLR4 ELISA Kits) signaling in the development of sepsis.
an important role for Cavin1 in lung homeostasis
This gene encodes a protein that enables the dissociation of paused ternary polymerase I transcription complexes from the 3' end of pre-rRNA transcripts. This protein regulates rRNA transcription by promoting the dissociation of transcription complexes and the reinitiation of polymerase I on nascent rRNA transcripts. This protein also localizes to caveolae at the plasma membrane and is thought to play a critical role in the formation of caveolae and the stabilization of caveolins. This protein translocates from caveolae to the cytoplasm after insulin stimulation. Caveolae contain truncated forms of this protein and may be the site of phosphorylation-dependent proteolysis. This protein is also thought to modify lipid metabolism and insulin-regulated gene expression. Mutations in this gene result in a disorder characterized by generalized lipodystrophy and muscular dystrophy.
polymerase I and transcript release factor
, leucine zipper protein
, leucine-zipper protein
, polymerase I and transcript release factor-like
, RNA polymerase I and transcript release factor
, TTF-I interacting peptide 12