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Mouse Anti-NEDD9 (Center) Recombinant Antibody (CBFYH-2673) (CBMAB-H3723-FY)

This product is mouse antibody that recognizes NEDD9. The antibody CBFYH-2673 can be used for immunoassay techniques such as: ELISA, WB, IF, IP.
See all NEDD9 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBFYH-2673
Antibody Isotype
IgG2b, κ
Application
ELISA, WB, IF, IP

Basic Information

Immunogen
Synthetic peptide
Specificity
Human
Antibody Isotype
IgG2b, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
0.02 M Potassium phosphate, 0.15 M NaCl, pH 7.2
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.
Epitope
Center

Target

Full Name
Neural Precursor Cell Expressed, Developmentally Down-Regulated 9
Introduction
The protein encoded by this gene is a member of the CRK-associated substrates family. Members of this family are adhesion docking molecules that mediate protein-protein interactions for signal transduction pathways. This protein is a focal adhesion protein that acts as a scaffold to regulate signaling complexes important in cell attachment, migration and invasion as well as apoptosis and the cell cycle. This protein has also been reported to have a role in cancer metastasis. Alternative splicing results in multiple transcript variants.
Entrez Gene ID
4739
UniProt ID
Q14511
Alternative Names
Neural Precursor Cell Expressed, Developmentally Down-Regulated 9; Cas Scaffolding Protein Family Member 2; Neural Precursor Cell Expressed Developmentally Down-Regulated Protein 9; Renal Carcinoma Antigen NY-REN-12; CAS-L; CASS2; HEF1; CASL; Crk-Associated Substrate Related Protein Cas-L; CRK-Associated Substrate-Related Protein
Function
Docking protein which plays a central coordinating role for tyrosine-kinase-based signaling related to cell adhesion. May function in transmitting growth control signals between focal adhesions at the cell periphery and the mitotic spindle in response to adhesion or growth factor signals initiating cell proliferation. May play an important role in integrin beta-1 or B cell antigen receptor (BCR) mediated signaling in B- and T-cells. Integrin beta-1 stimulation leads to recruitment of various proteins including CRK, NCK and SHPTP2 to the tyrosine phosphorylated form. Required for correct adhesion and migration of T-cells (PubMed:17174122).
Biological Process
Actin filament bundle assembly Source: UniProtKB
Actin filament reorganization Source: GO_Central
Activation of GTPase activity Source: Ensembl
Cell adhesion Source: ProtInc
Cell cycle Source: UniProtKB-KW
Cell division Source: UniProtKB-KW
Cell migration Source: GO_Central
Cytoskeleton organization Source: UniProtKB
Integrin-mediated signaling pathway Source: UniProtKB
Positive regulation of cell migration Source: UniProtKB
Positive regulation of protein tyrosine kinase activity Source: UniProtKB
Positive regulation of substrate adhesion-dependent cell spreading Source: UniProtKB
Regulation of growth Source: UniProtKB-KW
Signal transduction Source: ProtInc
Transmembrane receptor protein tyrosine kinase signaling pathway Source: GO_Central
Cellular Location
Cytoplasm
Nucleus
Golgi apparatus
Other locations
cell cortex
lamellipodium
focal adhesion
Note: Localizes to both the cell nucleus and the cell periphery and is differently localized in fibroblasts and epithelial cells. In fibroblasts is predominantly nuclear and in some cells is present in the Golgi apparatus. In epithelial cells localized predominantly in the cell periphery with particular concentration in lamellipodia but is also found in the nucleus. Isoforms p105 and p115 are predominantly cytoplasmic and associate with focal adhesions while p55 associates with mitotic spindle.
Enhancer of filamentation 1 p55:
Cytoskeleton
spindle
PTM
Cell cycle-regulated processing produces four isoforms: p115, p105, p65, and p55. Isoform p115 arises from p105 phosphorylation and appears later in the cell cycle. Isoform p55 arises from p105 as a result of cleavage at a caspase cleavage-related site and it appears specifically at mitosis. The p65 isoform is poorly detected.
PTK2/FAK1 phosphorylates the protein at the YDYVHL motif (conserved among all cas proteins). The SRC family kinases (FYN, SRC, LCK and CRK) are recruited to the phosphorylated sites and can phosphorylate other tyrosine residues. Ligation of either integrin beta-1 or B-cell antigen receptor on tonsillar B-cells and B-cell lines promotes tyrosine phosphorylation and both integrin and BCR-mediated tyrosine phosphorylation requires an intact actin network. In fibroblasts transformation with oncogene v-ABL results in an increase in tyrosine phosphorylation. Transiently phosphorylated following CD3 cross-linking and this phosphorylated form binds to CRK and C3G. A mutant lacking the SH3 domain is phosphorylated upon CD3 cross-linking but not upon integrin beta-1 cross-linking. Tyrosine phosphorylation occurs upon stimulation of the G-protein coupled C1a calcitonin receptor. Calcitonin-stimulated tyrosine phosphorylation is mediated by calcium- and protein kinase C-dependent mechanisms and requires the integrity of the actin cytoskeleton. Phosphorylation at Ser-369 induces proteasomal degradation.

Hu, Z., Wei, F., Su, Y., Wang, Y., Shen, Y., Fang, Y., ... & Chen, Y. (2023). Histone deacetylase inhibitors promote breast cancer metastasis by elevating NEDD9 expression. Signal Transduction and Targeted Therapy, 8(1), 11.

Deneka, A. Y., Nikonova, A. S., Lee, H. O., Kruger, W. D., & Golemis, E. A. (2022). NEDD9 sustains hexokinase expression to promote glycolysis. Oncogenesis, 11(1), 15.

Deneka, A. Y., Kopp, M. C., Nikonova, A. S., Gaponova, A. V., Kiseleva, A. A., Hensley, H. H., ... & Golemis, E. A. (2021). Nedd9 Restrains Autophagy to Limit Growth of Early Stage Non–Small Cell Lung Cancer. Cancer research, 81(13), 3717-3726.

Alba, G. A., Samokhin, A. O., Wang, R. S., Zhang, Y. Y., Wertheim, B. M., Arons, E., ... & Maron, B. A. (2021). NEDD9 is a novel and modifiable mediator of platelet–endothelial adhesion in the pulmonary circulation. American journal of respiratory and critical care medicine, 203(12), 1533-1545.

Hua, S., Feng, T., Yin, L., Wang, Q., & Shao, X. (2021). NEDD9 overexpression: Prognostic and guidance value in acute myeloid leukaemia. Journal of cellular and molecular medicine, 25(19), 9331-9339.

Samokhin, A. O., Hsu, S., Paul, B. Y., Waxman, A. B., Alba, G. A., Wertheim, B. M., ... & Maron, B. A. (2020). Circulating NEDD9 is increased in pulmonary arterial hypertension: a multicenter, retrospective analysis. The Journal of Heart and Lung Transplantation, 39(4), 289-299.

Meng, H., Wu, J., Huang, Q., Yang, X., Yang, K., Qiu, Y., ... & Qi, H. (2019). NEDD9 promotes invasion and migration of colorectal cancer cell line HCT116 via JNK/EMT. Oncology Letters, 18(4), 4022-4029.

Gu, Y., Lu, J., Chen, C., & Zheng, F. (2019). NEDD9 overexpression predicts poor prognosis in solid cancers: a meta-analysis. OncoTargets and therapy, 12, 4213.

Zhao, S., Min, P., Liu, L., Zhang, L., Zhang, Y., Wang, Y., ... & Gu, L. (2019). NEDD9 facilitates hypoxia-induced gastric cancer cell migration via MICAL1 related Rac1 activation. Frontiers in pharmacology, 10, 291.

Jurčić, P., Radulović, P., Balja, M. P., Milošević, M., & Krušlin, B. (2019). E‑cadherin and NEDD9 expression in primary colorectal cancer, metastatic lymph nodes and liver metastases. Oncology Letters, 17(3), 2881-2889.

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For research use only. Not intended for any clinical use.

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