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The cell surface trafficking of PDIA1, PDIA3, and PDIA6 is dependent on KDELR1, which travels in a dynamic manner to the cell surface. This transport is assumed to result in PDI cell surface association, which differs from PDI inducible secretion into the extracellular space.
Elevated reactive oxygen species levels in hepatocellular carcinoma modulate cytoplasmic PDIA3 levels, resulting in hepatocellular carcinoma cell survival through DKC1 up-regulation
Study shows that ERp57 is highly expressed in the paclitaxelresistant ovarian cancer cell lines and provide evidence that ERp57 is associated with drug resistance in ovarian cancer.
The results imply that ERp57 has a protective role against pathological events induced by mutant SOD1 and they link ERp57 to the misfolding of TDP-43 in amyotrophic lateral sclerosis.
Data suggest that disulfide bond switch in allosteric activation/inactivation of TGM2 is example of post-translational redox regulation that is reversibly and allosterically modulated by two proteins (ERp57 and TRX). (TGM2 = transglutaminase 2; ERp57 = endoplasmic reticulum resident protein 57; TRX = thioredoxin-1)
Study demonstrated that the expression of PDIA3 is frequently upregulated at the mRNA and protein levels in diffuse gliomas. Its high expression was significantly correlated with high Ki-67, more TP53 mutations and poor survival outcome. These findings imply that high expression of PDIA3 plays an important role in diffuse glioma progression.
summarize available knowledge of ERp57's functions in subcellular compartments and the roles of dysregulated ERp57 in various diseases.
ERp57 is involved in sperm capacitation and spermatozoa-zona pellucida binding.
Thiol isomerase ERp57 is mobilized to the surface of activated platelets via a process that requires actin polymerization.
Findings suggested that miR-330-5p represents a potential tumor-suppressive miRNA and plays an important role in cutaneous malignant melanoma progression by suppressing TYR and PDIA3 expression.
Our study found increased expression of ERp57 in chronic hepatitis B -hepatocellular carcinoma (HBV-HCC) genesis. Such altered expression could be related to HBV infection and high ERp57 expression may lead to poor prognosis of HBV-HCC patients.
The interaction of different flavonoids with PDIA3 was investigated by quenching fluorescence analysis and the effects on protein activity were evaluated.
Upregulation of PDIA3 promotes ovarian cancer cell proliferation and migration.
Data show that knockdown of endoplasmic reticulum resident protein 57 (ERP57) expression resulted in increase in shikonin induced apoptosis, and suggest that ERP57 might be a therapeutic option for the treatment of acute myeloid leukemia.
Amyotrophic lateral sclerosis-linked PDIA3 mutations disrupt motor neuron connectivity.
These data indicate that the presence of autoantibodies to PDIA3 favors the development of an efficient and specific T-cell response against PDIA3 in colorectal cancer patients.
ERp57 levels are increased in the airway epithelium of asthmatic patients and in mice with allergic airways disease.
LEDGF/p75 Overexpression Attenuates Oxidative Stress-Induced Necrosis and Upregulates the Oxidoreductase ERP57/PDIA3/GRP58 in Prostate Cancer
it is possible that the vimentin and PDIA3 could be the candidate biomarkers specific to Achyranthes saponin therapy for rheumatoid arthritis in synovial membrane.
ERp57 specifically contributes to peripheral nerve regeneration, whereas its activity is dispensable for the survival of a specific neuronal population of the central nervous system.
These results suggest that Tat-PDIA3 could be used to protect spinal cord neurons from ischemic damage, due to its modulatory action on the oxidative/anti-oxidative balance. Tat-PDIA3 could be applicable to protects neurons from the ischemic damage induced by thoracoabdominal aorta obstruction.
Role of the ERp57 protein (1,25D3-MARRS receptor) in murine mammary gland growth and development
PDI knockout inhibits the inflammatory function of macrophages by decreasing ROS production and inactivating NF-kappaB pathway.
results demonstrate that the core circadian gene Clock regulates bone formation via transcriptional control of 1,2,5(OH)2D3 receptor PDIA3
These data indicate a synergistic crosstalk between 1alpha,25(OH)2D3 and BMP2 toward osteogenesis and mineral deposition, involving both VDR and Pdia3.
ERp57 deficiency causes neuromuscular defects
Data suggest that regulation of Pdia3 (protein disulfide isomerase associated 3 protein) expression by microRNA-330-5p is important in maintaining hair cycle through regulation of proliferation and migration capability of keratinocytes.
All the growth plate and bone abnormalities, however, become attenuated after the pubertal growth spurt, when protein synthesis is decelerated and, hence, ERp57 function is less essential.
a Wnt/beta-catenin-driven functional role of ENO1 and PDIA3 in alveolar epithelial cell plasticity in lung injury and repair, is reported.
ERp57 regulates thrombosis via multiple targets.
These data suggest the 25D3 -MARRS receptor/PDIA3/ERp57 may contribute to the length of lifespan in mammals.
Pdia3+/- mice exhibit a mild skeletal phenotype characterized by enlarged growth plates, reduced tether and trabecular bone formation, and impaired osteogenic potential of calvarial osteoblasts in vitro.
results suggest that both of PDI and PDIA3 possess Bak-dependent proapoptotic function through inducing mitochondrial outer membrane permeabilization, which provides a new mechanism linking ER chaperone proteins and apoptotic signaling
Maternal PDIA3 plays a crucial role in sperm decondensation by reducing protamine disulfide bonds in porcine oocytes, supporting its utility as a potential tool for oocyte selection in assisted reproduction techniques.
Cell cycle analyses demonstrated that the suppressed expression of ERp57 increased the sub-G1 population. These data reveal that increased expression of ERp57 may contribute to the protection from beta cell death caused by autophagic failure.
The current study implicates PDIA3 to be an important cellular neuroprotective mechanism against a toxic drug
Pdia3 co-localizes with vitamin D receptor and caveolin-1 on the surface of MC3T3-E1 osteoblasts. In response to 1alpha,25(OH)2D3, receptors translocate and change interactions.
These data indicate that both the chaperone functional domains and the subcellular location of Pdia3 control rapid membrane responses to 1alpha,25-dihydroxyvitamin d3.
PDIA3 may play in the progression of heart failure.
This gene encodes a protein of the endoplasmic reticulum that interacts with lectin chaperones calreticulin and calnexin to modulate folding of newly synthesized glycoproteins. The protein was once thought to be a phospholipase\; however, it has been demonstrated that the protein actually has protein disulfide isomerase activity. It is thought that complexes of lectins and this protein mediate protein folding by promoting formation of disulfide bonds in their glycoprotein substrates.
58 kDa glucose-regulated protein
, 58 kDa microsomal protein
, ER protein 57
, ER protein 60
, disulfide isomerase ER-60
, endoplasmic reticulum P58
, endoplasmic reticulum resident protein 57
, endoplasmic reticulum resident protein 60
, glucose regulated protein, 58kDa
, phospholipase C-alpha
, protein disulfide isomerase-associated 3
, protein disulfide-isomerase A3
, glucose regulated protein 58
, endoplasmic reticulum protein
, glucose regulated protein, 58 kDa
, phospholipase C, alpha
, ER-60 protease
, oxidoreductase ERp57
, protein disulfide isomerase associated 3
, glucose regulated protein 58kD
, 1,25D3-MARRS protein
, 1,25D3-membrane-associated, rapid-response steroid-binding protein
, 25D3-MARRS protein
, glucose regulated thiol oxidoreductase protein
, glucose-regulated thiol oxidoreductase 58 kDa protein
, rapid-response steroid-binding protein
, glucose regulated protein
, protein disulfide isomerase family A member 3 S homeolog
, protein disulfide isomerase family A, member 3