Mouse anti-Human NRP1 monoclonal antibody (CABT-B12289)


Host Species
Antibody Isotype
Species Reactivity


Application Notes
The recommended antibody dilution for labeling of cells and subsequent analysis by flow cytometry is 1:11
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.


Entrez Gene ID
UniProt ID


Have you cited CABT-B12289 in a publication? Let us know and earn a reward for your research.

Custom Antibody Labeling

We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More

Customer Reviews

Write a review, share your experiences with others and get rewarded !
Product Name Cat. No. Applications Host Species Datasheet Price Add to Basket
Mouse IgG1 Isotype Control DAGIC1206 FC ELISA ICC IHC Mouse PDF Inquiry


MicroRNA-9 suppresses cancer proliferation and cell cycle progression in acute lymphoblastic leukemia with inverse association of neuropilin-1


Authors: Zang, Yuzhu; Yu, Runhong; Bai, Yanliang; Chen, Xiangli

Acute lymphoblastic leukemia (ALL) is one of the most common and most malign childhood cancers. In this work, we investigated the expression and function of human mature microRNA-9 (miR-9) in ALL. In ALL in vitro cell lines and in situ clinical specimens, gene expression of miR-9 was tested by qRT-PCR. MiR-9 was overexpressed in CEM/C1 and Molt-3 cells to investigate its possible anti-cancer effects on ALL in vitro proliferation, cell-cycle progression, and in vivo explant growth. The possible downstream target of miR-9, neuropilin-1 (NRP1), was examined by dual-luciferase activity assay, qRT-PCR, and Western blot. NRP1was upregulated in miR-9-overexpressed CEM/C1 and Molt-3 cells to investigate the functional involvement of NRP1 in miR-9-mediated regulation on ALL in vitro proliferation and cell-cycle progression. MiR-9 was downregulated in ALL cell lines and leukemic T-cells of ALL patients. Lentivirus-mediated miR-9 overexpression inhibited ALL in vitro proliferation, cell-cycle progression, and in vivo explant growth. NRP1 was confirmed be the downstream target of miR-9, and inversely modulated by miR-9 in ALL. NRP1 upregulation reversed the anti-cancer regulations of miR-9 on ALL in vitro proliferation and cell-cycle progression. MiR-9 is downregulated in ALL. Overexpressing miR-9 may inhibit ALL development, possible through its downstream target of NRP1.

HLX affects cell cycle and proliferation in AML cells via the JAK/STAT signaling pathway


Authors: Zhu, Xia-Yin; Guo, Qun-Yi; Zhu, Min; Chen, Bao-Guo; Wang, Ling-Yan; Zhang, Dan-Qiong; Zhang, Li; Shao, Yan-Ping; Luo, Wen-Da

Acute myelogenous leukemia (AML) is a class of malignant tumors derived from hematopoietic stem or progenitor cells. The H2.0-like homeobox gene (HLX) encodes transcription factors that function in promoting normal hematopoietic cell proliferation and tumor immunity. The present study analyzed the effect of downregulating the HLX on cell cycle distribution and cell proliferation in AML. Moreover, the current study detected changes in the expression of genes and proteins in the Janus kinase (JAK)/STAT signaling pathway to investigate the mechanism of the action of HLX in tumor immunity in AML. HLX expression in AML cell lines was silenced using small interfering siRNA, and MTS/PMS-assay colorimetric assays were used to assess the effect of knockdown of HLX on AML cell proliferation. Flow cytometry was used to analyze changes in cell cycle distribution, while reverse transcription-quantitative PCR and western blotting were used to detect changes in the expression levels of key components of the JAK/STAT signaling pathway, such as p21-activated kinase 1 (PAK1), neuropilin 1 (NRP1), B-cell translocation gene 1 (BTG1) and STAT5. It was found that HLX was differentially expressed in AML cell lines of various subtypes, and HLX expression was higher in the AML/M3 subtype NB4 cell line compared with the control group. Knockdown of HLX in NB4 cells significantly inhibited cell proliferation and arrested cells in the G(0)/G(1) phase. Moreover, STAT5 protein expression, as well as NRP1 and PAK1 expression levels were downregulated, while BTG1 expression was upregulated when HLX was knocked out by siRNA. Collectively, the results suggested that downregulation of HLX may cause G(0)/G(1) phase arrest and inhibit the proliferation of AML cells by activating the JAK/STAT signaling pathway.

Online Inquiry

Phone: *
E-mail Address: *
Technology Interest:
Type of Organization:
Service & Products Interested: *
Project Description:

Related Products

Related Resources

Ordering Information

Payment methods we support:
Invoice / Purchase Order
Credit card

Inquiry Basket