Ignet
Search (e.g., vaccine, IFNG): Help
About
Home
Introduction
Statistics
Programs
Dignet
Gene
GenePair
BioSummarAI
Help & Docs
Documents
Help
FAQs
Links
Acknowledge
Disclaimer
Contact Us
UM Logo

UMMS Logo

UMMS Logo

Gene Information

Gene symbol: PDIA2

Gene name: protein disulfide isomerase family A, member 2

HGNC ID: 14180

Synonyms: PDA2, PDI, PDIR

Related Genes

# Gene Symbol Number of hits
1 ATF4 1 hits
2 ATF6 1 hits
3 BCL2L11 1 hits
4 BNIP3L 1 hits
5 CALR 1 hits
6 CANX 1 hits
7 CDC2L1 1 hits
8 CPB1 1 hits
9 EDEM1 1 hits
10 EIF2AK3 1 hits
11 EIF2S1 1 hits
12 ERN1 1 hits
13 HSP90B1 1 hits
14 HSPA5 1 hits
15 HYOU1 1 hits
16 IDDM2 1 hits
17 IDE 1 hits
18 INS 1 hits
19 MAPK1 1 hits
20 MAPK8 1 hits
21 P4HB 1 hits
22 PDIA3 1 hits
23 PIK3CA 1 hits
24 PPP1R15A 1 hits

Related Sentences

# PMID Sentence
1 1692206 The higher expression of rat PDI mRNA in diabetes is due to an increase in the transcriptional rate of the gene, and insulin treatment of diabetic animals produces within 30 min a decrease in the level of transcription of PDI gene, as judged by nuclear run-on transcription experiments performed in vivo.
2 9793760 Most evidence supports IDE as the primary degradative mechanism, but other systems (PDI, lysosomes, and other enzymes) undoubtedly contribute to insulin metabolism.
3 9793760 IDE increases proteasome and steroid hormone receptor activity, and this activation is reversed by insulin.
4 9793760 This raises the possibility of a direct intracellular interaction of insulin with IDE that could modulate protein and fat metabolism.
5 11891612 In patients with insulin-dependent diabetes mellitus (IDDM) isolated peripheral airway involvement may give rise to inspiratory threshold load (ITL) contributing to dyspnea.
6 11891612 In this subset of patients with IDDM, Edi/Pdi ratio throughout increase in EELV and ITL was found to affect the perception of dyspnea in hypoxia to a similar extent as in hypercapnia.
7 15952740 A number of proteins identified in this study (e.g., annexin A2, elongation factor 1-alpha 2, histone H2B.a/g/k, heat shock protein 90 beta, heat shock 27 kDa protein, cyclophilin B, peroxiredoxin 4, cytokeratins 7, 18, and 19) have not been previously described in the database of mouse pancreatic islets.
8 15952740 In addition, altered expression of several proteins, like GRP78, GRP94, PDI, calreticulin, annexin, cytokeratins, profilin, heat shock proteins, and ORP150 have been associated with the development of diabetes.
9 16023999 This change was reflected by a significant increase in the total- and protein-sulfhydryl content, as well as in the free sulfhydryl groups of the major protein disulfide isomerases (PDIs), the 58 kDa PDI and the 57 kDa ERp57 but not other chaperones.
10 16601139 INS-1 cells exposed to palmitate for 16-24 h under serum-free conditions showed marked apoptosis and increased protein levels of phosphorylated eukaryotic translation initiation factor 2alpha (eIF2alpha), activating transcription factor 4 (ATF4), X box-binding protein 1 (XBP-1), and C/EBP homologous transcription factor (CHOP) compared with control cells.
11 16601139 Unexpectedly, the levels of the ER chaperone proteins Grp78/BiP and PDI were not affected by palmitate treatment, suggesting that the cell protective aspects of the unfolded protein response (UPR) are not up-regulated by palmitate.
12 16628255 Remarkably, acinar cells rather than beta cell islets were the major targets of autoimmune destruction in Aire-deficient NOD mice, and this alteration of intra-pancreatic target-organ specificity was associated with production of autoantibody against pancreas-specific protein disulfide isomerase (PDIp), an antigen expressed predominantly by acinar cells.
13 21475143 Examined were the effects of intravenously infused glucose and/or lipids on proximal ER stress sensor activation (PERK, eIF2-α, ATF4, Xbox protein 1 (XBP1s)), unfolded protein response (UPR) proteins (GRP78, calnexin, calreticulin, protein disulphide isomerase (PDI), stress kinases (JNK, p38 MAPK) and insulin signaling (insulin/receptor substrate (IRS) 1/2 associated phosphoinositol-3-kinase (PI3K)) in rat liver.
14 21475143 Glucose and/or lipid infusions, ranging from 23.8 to 69.5 kJ/4 h (equivalent to between ~17% and ~50% of normal daily energy intake), activated the proximal ER stress sensor PERK and ATF6 increased the protein abundance of calnexin, calreticulin and PDI and increased two GRP78 isoforms.
15 21475143 Glucose and glucose plus lipid infusions induced comparable degrees of ER stress, but only infusions containing lipid activated stress kinases (JNK and p38 MAPK) and inhibited insulin signaling (PI3K).
16 21475143 Examined were the effects of intravenously infused glucose and/or lipids on proximal ER stress sensor activation (PERK, eIF2-α, ATF4, Xbox protein 1 (XBP1s)), unfolded protein response (UPR) proteins (GRP78, calnexin, calreticulin, protein disulphide isomerase (PDI), stress kinases (JNK, p38 MAPK) and insulin signaling (insulin/receptor substrate (IRS) 1/2 associated phosphoinositol-3-kinase (PI3K)) in rat liver.
17 21475143 Glucose and/or lipid infusions, ranging from 23.8 to 69.5 kJ/4 h (equivalent to between ~17% and ~50% of normal daily energy intake), activated the proximal ER stress sensor PERK and ATF6 increased the protein abundance of calnexin, calreticulin and PDI and increased two GRP78 isoforms.
18 21475143 Glucose and glucose plus lipid infusions induced comparable degrees of ER stress, but only infusions containing lipid activated stress kinases (JNK and p38 MAPK) and inhibited insulin signaling (PI3K).
19 23638076 Compared with healthy blood donors, diabetic patients showed a profound decrease in both NKG2D-positive NK cells (44% vs. 55.5%, P<0.01) and NKp46-positive cells (26% vs. 50%, P<0.01).
20 23638076 Furthermore, markers of the Unfolded Protein Response (UPR) BiP, PDI and sXBP1 mRNAs were significantly increased in NK cells from T2D patients (P<0.05, P<0.01, P<0.05, respectively), indicating that ER stress is activated in vivo through both PERK and IRE1 sensors.
21 23638076 These results demonstrate for the first time defects in NK cell-activating receptors NKG2D and NKp46 in T2D patients, and implicate the UPR pathway as a potential mechanism.
22 23860123 There was a reduction in expression of genes important for the maintenance of ER homeostasis (Bip, p58(IPK), Edem1, and calreticulin) and an increase in proapoptotic genes (Bim, Bid, Nix, Gadd34, and Pdia2).