Anti-CGB5 monoclonal antibody (CABT-32595RH)


Host Species
Antibody Isotype
Species Reactivity
A synthetic peptide corresponding to residues in Human CGB5.


Application Notes
WB: 1/1000 - 1/10000;
*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.


Alternative Names
CGB5; chorionic gonadotropin, beta polypeptide 5; HCG; CG beta; CGB3; Chorionic gonadotrophin chain beta
Entrez Gene ID
UniProt ID

Product Background

Gene summary
CGB5 (Chorionic Gonadotropin Beta Subunit 5) is a Protein Coding gene. Diseases associated with CGB5 include gestational trophoblastic tumor and invasive mole. Among its related pathways are Transport to the Golgi and subsequent modification and Peptide hormone metabolism. GO annotations related to this gene include hormone activity. An important paralog of this gene is TSHB. This gene is a member of the glycoprotein hormone beta chain family and encodes the beta 5 subunit of chorionic gonadotropin (CG). Glycoprotein hormones are heterodimers consisting of a common alpha subunit and an unique beta subunit which confers biological specificity. CG is produced by the trophoblastic cells of the placenta and stimulates the ovaries to synthesize the steroids that are essential for the maintenance of pregnancy. The beta subunit of CG is encoded by 6 genes which are arranged in tandem and inverted pairs on chromosome 19q13. 3 and contiguous with the luteinizing hormone beta subunit gene.
Antigen Description
This gene encodes a common acute lymphocytic leukemia antigen that is an important cell surface marker in the diagnosis of human acute lymphocytic leukemia (ALL). This protein is present on leukemic cells of pre-B phenotype, which represent 85% of cases of ALL. This protein is not restricted to leukemic cells, however, and is found on a variety of normal tissues. It is a glycoprotein that is particularly abundant in kidney, where it is present on the brush border of proximal tubules and on glomerular epithelium. The protein is a neutral endopeptidase that cleaves peptides at the amino side of hydrophobic residues and inactivates several peptide hormones including glucagon, enkephalins, substance P, neurotensin, oxytocin, and bradykinin. This gene, which encodes a 100-kD type II transmembrane glycoprotein, exists in a single copy of greater than 45 kb. The 5 untranslated region of this gene is alternatively spliced, resulting in four separate mRNA transcripts. The coding region is not affected by alternative splicing. Stimulates the ovaries to synthesize the steroids that are essential for the maintenance of pregnancy.
Glycoprotein hormones, organism-specific biosystem; Metabolism, organism-specific biosystem; Metabolism of amino acids and derivatives, organism-specific biosystem; Peptide hormone biosynthesis, organism-specific biosystem.


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Methylation Allelic Polymorphism (MAP) in Chorionic Gonadotropin beta 5 (CGB5) and Its Association with Pregnancy Success


Authors: Uuskuela, Liis; Rull, Kristiina; Nagirnaja, Liina; Laan, Maris

Context: Increased epigenetic variability in the placenta may have evolved in response to its role in mediating the conflicting demands of the mother and fetus. One essential guardian of early pregnancy maintenance is the placental hormone human chorionic gonadotropin (HCG). Objective: Among the four primate-specific duplicate HCG beta-coding genes, chorionic gonadotropin-beta 8 (CGB8) and chorionic gonadotropin-beta 5 (CGB5) jointly contribute 62-82% of the total HCG beta transcript pool. Because these genes share common features with known imprinted placenta-expressed loci, we addressed the role of epigenetic mechanisms affecting their action. Design and Subjects: Parental origin of CGB5 and CGB8 transcripts and promoter methylation patterns were addressed in trophoblastic tissues from 23 mother-offspring duos and nine mother-father-offspring trios including the following: 1) third-trimester normal delivery at term (n = 14), 2) first-trimester elective termination of uncomplicated pregnancy (n = 10), and 3) first-trimester recurrent (>= 3) miscarriage (n = 8). Results:A normal uncomplicated pregnancy was characterized by balanced, biallelic expression of CGB5 and CGB8. However, in three (two recurrent miscarriage and one early elective termination of uncomplicated pregnancy) of nine genetically informative cases of CGB5, monoallelic expression of maternal alleles and hemimethylated gene promoters were identified. Conclusion: Our finding may represent a novel methylation allelic polymorphism or gain of imprinting in CGB5 promoter leading to expressional silencing of paternal alleles and increasing susceptibility to pregnancy loss. Aberrant methylation patterns in placenta may result from random reprogramming defects affecting normal implantation process. Alternatively, methylation allelic polymorphism in the placenta favoring the failure of pregnancy may arise as a response to cellular stress caused by, in general, aneuploidy or conditions in placental-maternal interface. (J Clin Endocrinol Metab 96: E199-E207, 2011)

A circulating antibody panel for pretransplant prediction of FSGS recurrence after kidney transplantation


Authors: Delville, Marianne; Sigdel, Tara K.; Wei, Changli; Li, Jing; Hsieh, Szu-Chuan; Fornoni, Alessia; Burke, George W.; Bruneval, Patrick; Naesens, Maarten; Jackson, Annette; Alachkar, Nada; Canaud, Guillaume; Legendre, Christophe; Anglicheau, Dany; Reiser, Jochen; Sarwal, Minnie M.

Recurrence of focal segmental glomerulosclerosis (rFSGS) after kidney transplantation is a cause of accelerated graft loss. To evaluate pathogenic antibodies (Abs) in rFSGS, we processed 141 serum samples from 64 patients with and without primary rFSGS and 34 non-FSGS control patients transplanted at four hospitals. We screened about 9000 antigens in pretransplant sera and selected 10 Abs targeting glomerular antigens for enzyme-linked immunosorbent assay (ELISA) validation. A panel of seven Abs (CD40, PTPRO, CGB5, FAS, P2RY11, SNRPB2, and APOL2) could predict posttransplant FSGS recurrence with 92% accuracy. Pretransplant elevation of anti-CD40 Ab alone had the best correlation (78% accuracy) with rFSGS risk after transplantation. Epitope mapping of CD40 with customized peptide arrays and rFSGS sera demonstrated altered immunogenicity of the extracellular CD40 domain in rFSGS. Immunohistochemistry of CD40 demonstrated a differential expression in FSGS compared to non-FSGS controls. Anti-CD40 Abs purified from rFSGS patients were particularly pathogenic in human podocyte cultures. Injection of anti-CD40/rFSGS Ab enhanced suPAR (soluble urokinase receptor)-mediated proteinuria in wild-type mice, yet no sensitizing effect was noted in mice deficient in CD40 or in wild-type mice that received blocking Ab to CD40. In conclusion, a panel of seven Abs can help identify primary FSGS patients at high risk of recurrence before transplantation. Intrarenal CD40 (and possibly other specific glomerular antigens) is an important contributor to FSGS disease pathogenesis. Human trials of anti-CD40 therapies are warranted to evaluate their efficacy for preventing rFSGS and improving graft survival.

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