anti-serpin Peptidase Inhibitor, Clade H (Heat Shock Protein 47), Member 1, (Collagen Binding Protein 1) (SERPINH1) Anticorps

Mouse (Murine) serpin Peptidase Inhibitor, Clade H (Heat Shock Protein 47), Member 1, (Collagen Binding Protein 1) (SERPINH1) interaction partners

1. HSP47 on the platelet surface interacts with collagen, stabilizes platelet adhesion and increases collagen-mediated signalling to mediate thrombus formation and hemostasis.

2. Increased Hsp47 expression is associated with collagen-related disorders such as fibrosis, characterized by abnormal collagen accumulation, highlighting Hsp47's potential as a clinically relevant therapeutic target.

3. These results highlight a cascade of fibrosis in chronic GVHD; macrophage production of transforming growth factor beta mediates fibroblast differentiation to HSP47(+) myofibroblasts that produce collagen. VA-lip HSP47 represent a novel strategy to modulate fibrosis in chronic GVHD by targeting HSP47(+) myofibroblasts without inducing immunosuppression.

4. The HSP47 might exert influence on liver fibrosis via the regulation ofendothelin receptor A (ETAR) and endothelin receptor B (ETBR).

5. miR-29b can reduce collagen biosynthesis during skin wound healing likely via post-transcriptional inhibition of HSP47 expression.

6. HSP47 appears after a period of certain activities to repair damaged collagen fibers, and the activity was returned to a state of equilibrium at day 30 with significantly diminished expression. Thus, the results suggest that HSP47 is actively involved in homeostasis of periodontal tissue subjected to occlusal overload

7. Intradermal administration of siHSP47-nanoparticles effectively reduced HSP47 protein expression in skin to normal level.

8. 2014). Data show that the expression of heat shock protein 47 (HSP47) was increased in the scleroderma mouse model.

9. Deletion of Hsp47 caused activated hepatic stellate cells to undergo ER stress-mediated apoptosis when autophagy was inhibited

10. Mouse embryonic stem cell migration and differentiation into smooth muscle cells is induced by the over-expression of HSP47.

11. Authors conclude that heat shock protein 47 plays an essential role in Schistosoma japonicum-induced hepatic fibrosis in mice.

12. miR-29b down-regulates HSP47 and LOX expression.

13. expression patterns of HSP70 and HSP47 in tissues following short-pulse laser irradiation

14. The pH sensitivity of murine heat shock protein 47 (HSP47) binding to collagen is affected by mutations in the breach histidine cluster.

15. These results demonstrate that Hsp47 is indispensable for well-organized cartilage and normal endochondral bone formation.

16. overexpression of HSP47 in keloid fibroblast cells could induce excessive collagen accumulation by enhancing collagen synthesis, which not only presents a possible mechanism of keloid formation

17. alpha-smooth-muscle-actin-positive myofibroblast of bleomycin-induced pulmonary fibrosis cells may synthesize procollagen in the fibrotic process of bleomycin-treated lungs through upregulation of HSP47 mRNA and play an important role in fibrogenesis.

18. HSP47 localized in alpha-smooth muscle actin-positive myofibroblasts, F4/80 negative, surfactant protein-A-positive type II pneumocytes, and F4/80-positive macrophages. Cells may play role in fibrotic process through upregulation of HSP47.

19. Results indicate that Hsp47 is required for the molecular maturation of type IV collagen and suggest that misfolded type IV collagen causes abnormal morphology of embryoid bodies.

20. type IV collagen in dilated endoplasmic reticulum leads to apoptosis in Hsp47-knockout mouse embryos via induction of CHOP

Human serpin Peptidase Inhibitor, Clade H (Heat Shock Protein 47), Member 1, (Collagen Binding Protein 1) (SERPINH1) interaction partners

1. HSP47 on the platelet surface interacts with collagen, stabilizes platelet adhesion and increases collagen-mediated signalling to mediate thrombus formation and hemostasis.

2. Increased Hsp47 expression is associated with collagen-related disorders such as fibrosis, characterized by abnormal collagen accumulation, highlighting Hsp47's potential as a clinically relevant therapeutic target.

3. It could be concluded that LF is a promising antifibrotic drug and could be considered as one of the HSP47 inhibitors but SM is still more potent

4. SERPINH1 was directly regulated by the miR-29 family, and its overexpression was detected in renal cell carcinoma surgical specimens and tyrosine kinase inhibitor failure autopsy specimens. High expression of SERPINH1 was significantly associated with tumor stage, pathological grade and poor prognosis.

5. SERPINH1 is an independent precision predictor for unfavourable prognosis in clear cell renal cell carcinoma.

6. HSP47 a well-established endoplasmic reticulum-resident collagen chaperone, also binds decorin, lumican, and fibromodulin with affinities comparable with that in the Hsp47-type I collagen interaction.

7. Our present data suggest that HSP47 is an important prognostic factor and an attractive therapeutic target in laryngeal squamous cell carcinoma (LSCC)due to its influence on the biological behaviour of LSCC cells

8. an endoplasmic reticulum complex of resident chaperones that includes HSP47, FKBP65, and BiP regulating the activity of LH2.

9. These observations indicate that this system is appropriate for detecting the interaction between HSP47 and collagen, and could be applied to high-throughput screening for drugs capable of suppressing and/or curing fibrosis.

10. miR-29b can reduce collagen biosynthesis during skin wound healing likely via post-transcriptional inhibition of HSP47 expression.

11. HSP47 expression in patients with colorectal cancer and the number of HSP47-positive spindle cells in the tumor stroma were significantly higher compared with those in adjacent normal colonic mucosa, and the number of the latter cells increased with tumor progression.

12. The essential parts of the Golgi stress response from the perspective of the organelle autoregulation. The pathways of the mammalian Golgi stress response have been identified, specifically the HSP47 pathway.

13. Overexpression of LOXL2 and SERPINH1 was observed in clinical specimens of lung cancer and fibrotic lesions. Downregulation of miR-29a caused overexpression of LOXL2 and SERPINH1 in lung cancer and IPF, suggesting that these genes are involved in the pathogenesis of these two diseases.

14. The changes in the SERPINH1 and SERPINF1 genes in patients with osteogenesis imperfect were synonymous polymorphisms or missense changes located in non-coding regions.

15. Overexpression of HSP47 is associated with poor prognosis in patients with esophageal squamous cell carcinoma and this is consistent with the function of HSP47 in terms of increased cell proliferation and colony formation.

16. A novel homozygous variant in SERPINH1 associated with a severe, lethal presentation of osteogenesis imperfecta with hydranencephaly.

17. The present study demonstrates that HSP47 promotes glioma angiogenesis and highlights the importance of HSP47 as an attractive therapeutic target of GBM.

18. Although the chemical chaperone 4-PBA partially restores the solubility of the Hsp47 OI mutants, collagen-binding activity of Hsp47 was not improved.

19. Data show that the expression of heat shock protein 47 (HSP47) was increased in the peripheral blood mononuclear cells and plasma from scleroderma patients.

20. Mutations in the HSP47 and FKBP65 produce a moderately severe form of Osteogenesis imperfect.