Human SYPL1 blocking peptide (CDBP2894)

Synthetic Human SYPL1 blocking peptide for BL, WB

Product Overview
Blocking peptide for anti-SYPL1 antibody
Species Reactivity
Application Notes
For in vitro research use only. Not intended for any diagnostic or therapeutic purpose. Not suitable for human or animal consumption.
200 μg/ml
50 μg
PBS containing 0.02% sodium azide
0.02% Sodium Azide
Store at -20℃, stable for one year.
UniProt ID
Antigen Description
SYPL1 (synaptophysin-like 1) is a protein-coding gene. Diseases associated with SYPL1 include alcoholism, and neuronitis. GO annotations related to this gene include transporter activity. An important paralog of this gene is SYNPR.
transporter activity;
SYPL1; synaptophysin-like 1; synaptophysin like protein , SYPL; synaptophysin-like protein 1; pantophysin; SYPL; H-SP1;


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SYPL1 Inhibits Apoptosis in Pancreatic Ductal AdenocarcinomaviaSuppression of ROS-Induced ERK Activation


Authors: Song, Yunda; Sun, Xuesong; Duan, Fangting; He, Chaobin; Wu, Jiali; Huang, Xin; Xing, Kaili; Sun, Shuxin; Wang, Ruiqi; Xie, Fengxiao; Mao, Yize; Wang, Jun; Li, Shengping

Synaptophysin-like 1 (SYPL1) is a neuroendocrine-related protein. The role of SYPL1 in pancreatic ductal adenocarcinoma (PDAC) and the underlying molecular mechanism remain unclarified. Here, after analyzing five datasets (GSE15471, GSE16515, GSE28735, TCGA, and PACA-AU) and 78 PDAC patients from Sun Yat-sen University Cancer Center, we demonstrated that SYPL1 was upregulated in PDAC and that a high level of SYPL1 indicated poor prognosis. Bioinformatics analysis implied that SYPL1 was related to cell proliferation and cell death. To validate these findings, gain-of-function and loss-of-function experiments were carried out, and we found that SYPL1 promoted cell proliferationin vitroandin vivoand that it protected cells from apoptosis. Mechanistic studies revealed that sustained extracellular-regulated protein kinase (ERK) activation was responsible for the cell death resulting from knockdown of SYPL1. In addition, bioinformatics analysis showed that the expression of SYPL1 positively correlated with antioxidant activity. Reactive oxygen species (ROS) were upregulated in cells with SYPL1 knockdown and vice versa. Upregulated ROS led to ERK activation and cell death. These results suggest that SYPL1 plays a vital role in PDAC and promotes cancer cell survival by suppressing ROS-induced ERK activation.

SYPL1 overexpression predicts poor prognosis of hepatocellular carcinoma and associates with epithelial-mesenchymal transition


Authors: Chen, Dong-Han; Wu, Qiu-Wan; Li, Xiu-Dong; Wang, Shuang-Jia; Zhang, Zhi-Ming

Hepatocellular carcinoma (HCC) is the second leading cause of cancer mortality worldwide, which is mainly due to relapse and metastasis. Synaptophysin-like 1 (SYPL1), a member of SYP family proteins, exerts complicated functions, which prompted us to wonder whether SYPL1 contributed to HCC progress. Herein, we performed integrative experiments of quantitative real-time polymerase chain reaction (qRT-PCR), western blot analysis and immunohistochemistry (IHC), and found that SYPL1 overexpression in HCC tissues was closely correlated with several malignant clinicopathologic features of HCC. The results from IHC in serial sections of HCC tissues further indicated that SYPL1 expression was associated with epithelial-mesenchymal transition (EMT) biomarkers of HCC cells. Additionally, Kaplan-Meier survival analysis showed that SYPL1 overexpression was significantly associated with reduced overall survival (OS) (p<0.001) and disease-free survival (DFS) (p=0.002). Furthermore, univariate and multivariate Cox proportional hazards analysis identified SYPL1 as an independent prognostic factor for OS [ hazard ratio (HR), 2.443, 95% confidence interval (CI), 1.429-4.177, p=0.001] and DFS (HR, 1.680, 95% CI=1.012-2.788, p=0.045) of HCC patients. Collectively, SYPL1 overexpression predicts poor prognosis of HCC and may associate with EMT of HCC cells. Therefore, SYPL1 could serve as a future novel biomarker and potential therapy target for HCC.

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