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Human Dipeptidyl-Peptidase 4 (DPP4) interaction partners

1. Data on CD26/dipeptidyl peptidase IV (CD26)-mediated immune regulation suggest that CD26 may be an appropriate therapeutic target for the treatment of selected immune disorders [Review].

2. Study provides mechanistic insights into the molecular interaction between KLK5 and DPP4 as well as CD4+ T cell derived KLK5 mediated enzymatic cleavage of DPP4 from cell surface. Study uncovers a hitherto unknown cellular source and mechanism behind enhanced plasma DPP4 activity in T2DM.

3. The elevated circulatory DPP4 levels in metabolic diseases.[review]

4. Our results showed 14% inferior plasma DPP-4 activity in adolescent idiopathic scoliosis (AIS) patients when compared to healthy controls . Similarly, osteoblasts derived from AIS subjects had lower DPP-4 gene and protein expression than controls by 90.5% and 57.1% respectively (P < 0.009). DPP-4 expression was regulated in a different manner in osteoblasts isolated from AIS participants compared to controls.

5. Here we review the recent advances in identifying the cellular sources of both circulating and membrane-bound DPP4 important for cleavage of the incretin hormones and regulation of glucose and lipoprotein metabolism.

6. DPP4 activity when compared to healthy controls. Analysis of Dpp4-Liv-Tg mice revealed elevated systemic DPP4 activity and diminished active GLP-1 levels.

7. DPP4 was not different in this group of polycystic ovarian syndrome patients. However, a relationship between DPP4 and markers of insulin resistance were found.

8. The analysis of their molecular properties allowed the design of a multiple linear regression model for activity prediction. Their docking analysis allowed visualization of the interactions between the pharmacophore regions and hDDP-IV.

9. The level of myocardial CD26 expression might be a predictive marker of prognosis in patients with heart failure.

10. Our study showed that complement was excessively activated in MERS-CoV-infected hDPP4-Tg mice through observations of increased concentrations of the C5a and C5b-9 complement activation products in sera and lung tissues, respectively.

11. API was demonstrated to inhibit the migration/invasion of NSCLC cells harboring different EGFR statuses via suppressing the Snail/Slug-mediated EMT..CD26 may be a useful biomarker for predicting NSCLC progression. API effectively suppressed lung cancer progression by targeting the CD26-Akt-Snail/Slug signaling pathway

12. hepatocyte DPP4 promotes visceral adipose tissue inflammation and insulin resistance in obesity, and targeting this pathway may have metabolic benefits that are distinct from those observed with oral DPP4 inhibitors

13. this study shows that CD26 expression is down-regulated on CD8(+) T cells in patients with Hashimoto's thyroiditis

14. Several isoforms of DPP-IV and FAP are present in glioblastoma tissue. The absence of alkaline isoforms of both enzymes in glioma cell lines however suggests that isoforms from other, most likely stromal, cell types contribute to the overall pattern seen in glioblastoma tissues.

15. Data suggest that dipeptidyl peptidase 4 (DPPIV) gene polymorphism influences disease susceptibility and acute pancreatitis (AP) severity.

16. High levels of DPP4a are independently associated with an increased rate of no-reflow events.

17. DPP-4 activity and GLP-1total levels were higher in patients with microvascular complications associated with T2DM. Contrary to expectations, no negative correlation was seen between GLP-1 and DDP-4 levels. This result suggests the possible inefficacy of DDP-4 activity as a marker to predict in vivo degradation of endogenous GLP-1.

18. The study showed that DPP-4 inhibitor use does not modify the risk of bone fracture compared with placebo or other anti-diabetic medications in patients with type 2 diabetes.

19. A close connection between SerpinB3 and DPPPIV has been identified, but further studies are required to better understand the mechanism by which these proteins communicate and exert metabolic effects in hepatocellular carcinoma.

20. There is a U-shaped association of serum DPP-IV with mortality in chronic heart failure patients.

Cow (Bovine) Dipeptidyl-Peptidase 4 (DPP4) interaction partners

1. Results describe a proline-rich cytokine from neurosecretory granules that represents a new natural substrate for Dipeptidyl Peptidase IV (DPPIV).

2. This and other dipeptidyl peptidases can be isolated from bovine testes.

3. Data demonstrate that dipeptidyl peptidase II can form a complex with adenosine deaminase, but with one order of magnitude higher dissociation constant than that of DPPIV.

Pig (Porcine) Dipeptidyl-Peptidase 4 (DPP4) interaction partners

1. This study shows that porcine DPP-IV is generally inhibited with greater potency by protein-derived peptides than is the human enzyme

2. DPP-IV from porcine kidney cortex was characterized.

3. Neutral endopeptidase 24.11 and DPP-IV is superior to DPP-IV inhibition alone in preserving intact GLP-1, which implies possibility that the combination has therapeutic potential.

4. Results describe the distribution of dipeptidyl peptidase IV-like activity enzymes in porcine tissue sections by RT-PCR.

Mouse (Murine) Dipeptidyl-Peptidase 4 (DPP4) interaction partners

1. These data indicate that DPP-4 is modulated in a tissue specific manner and is dependent on physiological conditions such as hyperglycaemia and insulin resistance, suggesting a significant role in disorders such as diabetes.

2. DPP4 activity when compared to healthy controls. Analysis of Dpp4-Liv-Tg mice revealed elevated systemic DPP4 activity and diminished active GLP-1 levels.

3. hepatocyte DPP4 promotes visceral adipose tissue inflammation and insulin resistance in obesity, and targeting this pathway may have metabolic benefits that are distinct from those observed with oral DPP4 inhibitors

4. DPP-4 inhibition with linagliptin slowed the progression of premature aging in klotho-/- mice. Provide a novel insight into the potential role of DPP-4 in the mechanism of premature aging.

5. Chronic stress accelerates DPP4-mediated GLP-1 degradation and alters plasma adiponectin, accelerating vascular senescence and impairing ischemia-induced neovascularization.

6. p53 limits ferroptosis of colorectal cancer cells by blocking DPP4 activity.

7. DPP4 can regulate chronic stress-induced hematopoietic stemc cell activation and inflammatory cell production via an Adrbeta3/CXCL12-dependent mechanism that is mediated by the GLP-1/GLP-1R axis.

8. DPPIV-knockout mice showed attenuation of scratching in psoriatic pruritus disease model.

9. Actions of several substrate chemokines might be potentiated by downregulation of DPP-4, synergistically with upregulation of chemokines and their receptors in adipose tissues of obese mice.

10. Inhibition of DPP-4 activity by linagliptin reverses Western diet-induced diastolic dysfunction, possibly by targeting TRAF3IP2 expression and its downstream inflammatory signaling.

11. DPP4 is pro-fibrotic in Carbon tetrachloride-induced liver fibrosis.

12. systemic DPP4 inhibition restores the impaired mononuclear cell homing in Eng+/- animals post-myocardial infarction, and enhances cardiac repair, which might be explained by restoring the balance between the inflammatory and regenerative macrophages present in the heart

13. SGLT-2 inhibition with dapagliflozin reduces the activation of the Nlrp3/ASC inflammasome and attenuates the development of diabetic cardiomyopathy in mice with type 2 diabetes. Effects are augmentated of the by DPP4 inhibitor Saxagliptin.

14. DPP-4 inhibitor teneligliptin inhibited atherogenesis in ApoE knockout mice, at least partially, through attenuation of the inflammatory phenotype of perivascular adipose tissue.

15. Increased plasma DPP-4 activity may correlate with aneurysmal development. CD26 on monocytes plays a critical role in cell differentiation, possibly mediated by extracellular signal-regulated protein kinase 1/2-p21 axis signaling pathways and cytoskeletal proteins reassembly.

16. High DPP4 expression is associated with cardiac ischemia and systolic dysfunction.

17. DPP4:CD9:TTSP as the protein complexes are necessary for early efficient MERS-coronavirus entry.

18. these findings identify distinct roles for DPP4 in the endothelial cell versus the bone marrow compartment for selective incretin degradation and DPP4 inhibition-mediated glucoregulation.

19. The trimeric form receptor-binding domain of MERS-CoV spike protein bound strongly to the receptor of MERS-CoV, dipeptidyl peptidase 4 (DPP4), and elicited robust RBD-specific neutralizing antibodies in mice.

20. the data show that glucose-induced expression of Dpp4 in the liver is facilitated by demethylation of the Dpp4 gene early in life. This might contribute to early deteriorations in hepatic function, which in turn result in metabolic disease such as hepatosteatosis later in life.