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Rabbit Anti-CEP55 Recombinant Antibody (EG651) (CBMAB-EN784-LY)


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Summary

Host Animal
Rabbit
Specificity
Human, Rat
Clone
EG651
Antibody Isotype
IgG
Application
IF, WB

Basic Information

Immunogen
A synthetic peptide of human CEP55.
Host Species
Rabbit
Specificity
Human, Rat
Antibody Isotype
IgG
Clonality
Monoclonal Antibody
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.
ApplicationNote
WB1:500-1:1,000
IF(ICC)1:50-1:200

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

Format
Liquid
Buffer
40% Glycerol, 0.05% BSA
Preservative
0.01% sodium azide
Concentration
Batch dependent
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Introduction
CEP55 (Centrosomal Protein 55) is a Protein Coding gene. Diseases associated with CEP55 include Multinucleated Neurons, Anhydramnios, Renal Dysplasia, Cerebellar Hypoplasia, And Hydranencephaly and Meckel Syndrome, Type 1. Among its related pathways are DNA Damage and Cytoskeletal Signaling.
Entrez Gene ID
55165
UniProt ID
Q53EZ4
Alternative Names
Centrosomal Protein 55; Up-Regulated In Colon Cancer 6; Cancer/Testis Antigen 111; Centrosomal Protein 55kDa; C10orf3; URCC6;
Function
Plays a role in mitotic exit and cytokinesis (PubMed:16198290, PubMed:17853893).
Recruits PDCD6IP and TSG101 to midbody during cytokinesis. Required for successful completion of cytokinesis (PubMed:17853893).
Not required for microtubule nucleation (PubMed:16198290).
Plays a role in the development of the brain and kidney (PubMed:28264986).
Biological Process
Cranial skeletal system development Source: UniProtKB
Establishment of protein localization Source: UniProtKB
Midbody abscission Source: UniProtKB
Mitotic cytokinesis Source: MGI
Multicellular organism development Source: UniProtKB-KW
Regulation of phosphatidylinositol 3-kinase signaling Source: InterPro
Cellular Location
Centriole; Centrosome; Cytoplasm; Cleavage furrow; Midbody ring. Present at the centrosomes at interphase. A small portion is associated preferentially with the mother centriole, whereas the majority localizes to the pericentriolar material. During mitosis, loses affinity for the centrosome at the onset of prophase and diffuses throughout the cell. This dissociation from the centrosome is phosphorylation-dependent. May remain localized at the centrosome during mitosis in certain cell types. Appears at the cleavage furrow in late anaphase and in the midbody in cytokinesis.
Involvement in disease
Multinucleated neurons, anhydramnios, renal dysplasia, cerebellar hypoplasia and hydranencephaly (MARCH): An autosomal recessive, congenital disease characterized by severe hydranencephaly with multinucleated neurons, renal aplasia or dysplasia, and hypoplastic kidneys. Hydranencephaly is an anomaly leading to replacement of the cerebral hemispheres with a fluid-filled cyst. MARCH results in death in utero or in the perinatal period.
PTM
There is a hierachy of phosphorylation, where both Ser-425 and Ser-428 are phosphorylated at the onset of mitosis, prior to Ser-436. Phosphorylation at Ser-425 and Ser-428 is required for dissociation from the centrosome at the G2/M boundary. Phosphorylation at the 3 sites, Ser-425, Ser-428 and Ser-436, is required for protein function at the final stages of cell division to complete cytokinesis successfully.
More Infomation

Huang, R. H., Yang, W. K., Wu, C. M., Yeh, C. M., & Sung, W. W. (2021). Over-expression of CEP55 predicts favorable prognosis in colorectal cancer patients with lymph node involvement. Anticancer Research, 41(1), 543-547.

Tandon, D., & Banerjee, M. (2020). Centrosomal protein 55: A new paradigm in tumorigenesis. European Journal of Cell Biology, 99(5), 151086.

Rawlins, L. E., Jones, H., Wenger, O., Aye, M., Fasham, J., Harlalka, G. V., ... & Baple, E. L. (2019). An Amish founder variant consolidates disruption of CEP55 as a cause of hydranencephaly and renal dysplasia. European Journal of Human Genetics, 27(4), 657-662.

Yanagi, K., Sone, R., Ohga, R., & Kawahara, A. (2019). Involvement of the centrosomal protein 55 (cep55) gene in zebrafish head formation. Genes to Cells, 24(10), 642-649.

Li, F., Jin, D., Guan, L., Zhang, C. C., Wu, T., Wang, Y. J., & Gao, D. S. (2019). CEP55 promoted the migration, invasion and neuroshpere formation of the glioma cell line U251. Neuroscience letters, 705, 80-86.

Ma, X. P., Zhang, W., Wu, B. Q., & Qin, J. (2018). Correlations between mRNA levels of centrosomal protein 55 (CEP55) and clinical features of patients with lung cancer. Medical science monitor: international medical journal of experimental and clinical research, 24, 3093.

Qi, J., Liu, G., & Wang, F. (2018). High levels of centrosomal protein 55 expression is associated with poor clinical prognosis in patients with cervical cancer. Oncology letters, 15(6), 9347-9352.

Zhu, H., Chen, D., Tang, J., Huang, C., Lv, S., Wang, D., & Li, G. (2018). Overexpression of centrosomal protein 55 regulates the proliferation of glioma cell and mediates proliferation promoted by EGFRvIII in glioblastoma U251 cells. Oncology letters, 15(2), 2700-2706.

Peng, T., Zhou, W., Guo, F., Wu, H. S., Wang, C. Y., Wang, L., & Yang, Z. Y. (2017). Centrosomal protein 55 activates NF-κB signalling and promotes pancreatic cancer cells aggressiveness. Scientific reports, 7(1), 1-12.

Jiang, W., Wang, Z., & Jia, Y. (2017). CEP55 overexpression predicts poor prognosis in patients with locally advanced esophageal squamous cell carcinoma. Oncology letters, 13(1), 236-242.

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

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