anti-UCHL1 (UCHL1) 抗体产品概述

Human Ubiquitin Carboxyl-terminal Esterase L1 (Ubiquitin Thiolesterase) (UCHL1) interaction partners

1. these results identified UCHL1 as a target podocyte protein of autoantibodies in a set of relapsing patients and support a causative role of anti-UCHL1 autoantibodies in the development of idiopathic steroid sensitive nephrotic syndrome

2. serum level not significantly elevated in newborns at risk for hypoxic ischemic encephalopathy but with normal EEGs

3. bserved significantly altered density of PGP 9.5-positive axonal nerve terminals in pruritic lesional and nonlesional psoriatic skin compared with controls;PGP 9.5 expression by suprabasal keratinocytes (SBKs) was significantly increased in itchy skin lesions compared to skin without itch.

4. This study demonstrated that UCHL1 expression is induced by HCV infection. UCHL1 stimulates JNK phosphorylation and signaling related to HSCs activation after binding to the cell surface of HSCs.

5. Study showed that UCHL1 could serve as a prognostic marker indicating a favorable clinical outcome in Neuroblastoma (NB). UCHL1 expression was higher in ganglioneuroblastomas/ganglioneuromas (GNB/ GN) and well-differentiated NB than poorly differentiated NB, and UCHL1 expression was strongly associated with differentiation markers, indicating the positive correlation between UCHL1 expression and NB differentiation.

6. The proteins UCH-L1 and alpha-internexin could be independent prognostic biomarkers of pancreatic neuroendocrine tumors.

7. We have also demonstrated that UCHL1 S-nitrosylation provides seeding for faster aggregation of a-synuclein. Finally, the in vitro nitrosylation of UCHL1 was corroborated with rotenone induced mouse model of PD

8. In newborns undergoing cardiac surgery, ubiquitin C-terminal hydrolase 1 showed a significant rise at 0 hours in the deep hypothermic circulatory arrest group compared to baseline. Levels returned to baseline at 12 hours. There was an early rise in UCHL1 at 0 hours in the cardiopulmonary bypass group.

9. Overexpression of UCHL1 genes promoted apoptosis in cells treated with VER+ADM. UCHL1 knockdown using siRNA weakened the effect of ADM+VER, indicating that ADM+VER promotes HCC cell apoptosis and that UCHL1 genes participate in VER-mediated promotion in tumor cell apoptosis.

10. Cholangiocarcinoma patients who had high methylation of HTATIP2 and low methylation of UCHL1 showed longer overall survival than those with low HTATIP2 methylation and high UCHL1 methylation.

11. High UCHL1 expression is associated with posterior longitudinal ligament ossification.

12. Prx II exhibited more effective molecular chaperone activity than Prx I when UCH-L1 was the client. Prx II interacted with UCH-L1 through its C-terminal region to protect UCH-L1 from thermal or oxidative inactivation

13. Data report that the expression of UCH-L1 is significantly higher in breast cancer cells with higher invasive ability. Also, the overexpression of UCH-L1 led to activation of Akt and phosphorylation. Thus, these findings demonstrated that UCH-L1 promotes invasion of breast cancer cells.

14. The authors observed higher serum levels of GFAP and UCH-L1 in brain-injured children compared with controls and also demonstrated a step-wise increase of biomarker concentrations over the continuum of severity from mild to severe traumatic brain injury. Serum UCH-L1 and GFAP concentrations also strongly predicted poor outcome.

15. UCHL1 inhibits autophagy and is depending on its de-ubiquitinating activity.

16. Uchl1 concentrations in the blood plasma of boys with cryptorchidism, may reflect the heat-induced apoptosis of germ cells

17. Overexpression of UCHL1 is associated with thermal injury.

18. UCHL1 localizes to TTAGGG repeats at telomeres and interstitial telomeric sequences. A weak or transient interaction between UCHL1 and the shelterin complex was confirmed by immunoprecipitation and proximity ligation assays.

19. novel biomarker for identifying malignant potential of primary well-differentiated and moderately differentiated pancreatic neuroendocrine tumors

20. detection of significantly higher levels of UCH-L1 in patients with ischemic stroke and intracranial hemorrhage compared to patients with metabolic disorder induced impaired consciousness and healthy volunteers

Pig (Porcine) Ubiquitin Carboxyl-terminal Esterase L1 (Ubiquitin Thiolesterase) (UCHL1) interaction partners

1. The elevation in UCH-L1 concentration is consistent with the severity of neural apoptosis following DHCA.

2. Data report that ubiquitin carboxy-terminal hydrolase 1 is expressed in spermatogonia located at the basement membrane of seminiferous tubules at high and low levels, but not in differentiated germ cells distant from the BM.

Cow (Bovine) Ubiquitin Carboxyl-terminal Esterase L1 (Ubiquitin Thiolesterase) (UCHL1) interaction partners

1. These data indicate that antipolyspermy defense in bovine oocytes may rely on UCHL1-controlled functioning of These data indicate that antipolyspermy defense in bovine oocytes may rely on UCHL1-controlled functioning of cortical granules.

Mouse (Murine) Ubiquitin Carboxyl-terminal Esterase L1 (Ubiquitin Thiolesterase) (UCHL1) interaction partners

1. UCH-L1 is required for regulated protein degradation in the kidney by controlling proteasome abundance. Altered proteasome abundance renders renal cells, particularly podocytes and endothelial cells, susceptible to injury.

2. High UCHL1 expression is associated with posterior longitudinal ligament ossification.

3. PKCgamma-mediated down-regulation of UCHL1 alleviates ischemic neuronal injuries by decreasing autophagy via ERK-mTOR pathway.

4. Post-transcriptional loss of UCHL1 following status epilepticus is deleterious to neuronal survival.

5. The UCHL1 may play a role in myogenesis by promoting myoblast proliferation and inhibiting differentiation.

6. our study provides novel insights into the mechanisms of UCH-L1-mediated neurobiological functions and suggests that ubiquitination is an important regulatory signal for TrkB

7. Effects of Ubiquitin C-Terminal Hydrolase L1 (UCH-L1) inhibition on sperm incorporation and cortical tension in mouse eggs.

8. The neuronal marker UCH-L1 is induced in, and specifically augments the oncogene-induced transformation of, germinal center B cells.

9. Pharmacological inhibition of UCHL1 exacerbates rather than ameliorates disease symptoms in a mouse model of SMA. Thus, pharmacological inhibition of UCHL1 is not a viable therapeutic target for SMA.

10. Parkin mediates K63-linked polyubiquitination of UCH-L1 in cooperation with the Ubc13/Uev1a E2 ubiquitin-conjugating enzyme complex and promotes UCH-L1 degradation by the autophagy-lysosome pathway.

11. defective UCHL1 function may be an early contributor to vulnerability of pancreatic beta-cells for protein misfolding and proteotoxicity, hallmark defects in islets of T2DM

12. UCH-L1 facilitates PDGF-BB-induced suppression of autophagic degradation of p21WAF1/Cip1 proteins in cardiac fibroblasts

13. It plays a role in the hypothalamic-pituitary-gonadal axis and in the reproduction.

14. UCHL1 upregulation in ACTN4-associated FSGS.

15. downregulated miR-181b induces neuroprotection against ischemic injury through negatively regulating HSPA5 and UCHL1 protein levels

16. The proteases HtrA2/Omi and UCH-L1 regulate TNF-induced necroptosis.

17. Activation of the NF-kappaB signaling pathway could be the major pathogenic mechanism to up-regulate UCH-L1 in podocyte injury.

18. in AD, Abeta may down-regulate UCH-L1 in the AD brain, which in turn impairs BDNF/TrkB-mediated retrograde signaling, compromising synaptic plasticity and neuronal survival.

19. UCH-L1 physically interacts with CDK1, CDK4, and CDK5, enhancing their kinase activity.

20. UCH-L1 impairs mTORC1 activity toward S6 kinase and 4EBP1.

Horse (Equine) Ubiquitin Carboxyl-terminal Esterase L1 (Ubiquitin Thiolesterase) (UCHL1) interaction partners

1. There was no difference in enteric neuronal density and distribution in the groups of animals with intestinal disease compared with those without, apart from two (out of 28) horses with intestinal disease that showed reduction in PGP 9.5 immunoreactivity.