Characterization of mouse A33 antigen, a definitive marker for basolateral surfaces of intestinal epithelial cells

Abstract

The murine A33 antigen is emerging as a definitive marker of intestinal epithelial cells. Cloning and sequence determination of cDNAs encoding mA33 antigen predict a novel type 1 transmembrane protein of 298 amino acids, comprising an extracellular domain with two immunoglobulin-like domains, a single-span transmembrane domain, and a highly acidic cytoplasmic domain. On the basis of conservation of amino acid sequence and genomic structure, the mA33 antigen is a member of a growing subfamily within the immunoglobulin superfamily, which includes transmembrane proteins CTX/ChT1, CTM/CTH, and CAR. During embryonic development, mA33 antigen expression is first observed in the inner cell mass of blastocysts before implantation. Intestinal expression of mA33 antigen is initiated in the hindgut at E14.5 and increases steadily throughout late embryonic and postnatal life into adulthood. The protein is specifically expressed on the basolateral surfaces of intestinal epithelial cells of all lineages, independent of their position along the rostrocaudal and crypt-villus axes. Thus the mA33 antigen appears to be a novel marker for both proliferating and differentiating intestinal epithelial cells.

Phase I Trial of 131I-huA33 in Patients with Advanced Colorectal Carcinoma

“…It is therefore regarded as part of a subfamily within the immunoglobulin superfamily, together with the transmembrane proteins CTX (corticothymocyte marker in Xenopus), CTM/CTH (mouse and human homologues of CTX) and CAR (Coxsackie and adenovirus receptor; ref. 7). Its structure is consistent with a putative role as a cell adhesion molecule or a novel cell surface receptor.…”

Stomach-Specific Activation of Oncogenic KRAS and STAT3-Dependent Inflammation Cooperatively Promote Gastric Tumorigenesis in a Preclinical Model

“…S4B). We also detected signs of pseudointestinal metaplasia within the tumor-adjacent glandular epithelium and in the adenomas, comprising prominent appearance of goblet-like cells alongside the induction of the intestinal marker gpA33 (30,31) and to a lesser extent of Cdx2 (Fig. 4C and D and Supplementary Fig.…”

The expression of genes involved in jejunal lipogenesis and lipoprotein synthesis is altered in morbidly obese subjects with insulin resistance

“…The study was undertaken in 45 morbidly obese subjects who underwent a Roux-en-Y gastric bypass, and were classified in three groups according to the homeostasis model assessment of insulin resistance (HOMA-IR) level: [11][12][13] 15 subjects with low HOMA-IR (HOMA-IRo4.7) (MO-low-IR), 15 subjects with high HOMA-IR (HOMA-IR44.7) (MO-high-IR) (both groups without treatment for T2DM), and 15 subjects with T2DM who were only receiving metformin treatment (MO-metf-T2DM). Subjects were excluded if they had T2DM with insulin treatment, had cardiovascular disease, acute inflammatory or infectious disease, or were receiving drugs that could alter the lipid profile or the metabolic parameters at the time of inclusion in the study.…”

“…Subsequently, cells were washed twice with PBS and the number and frequency of IEC was determined by flow cytometry. Cells were kept on ice during 30 min and then were incubated with a rat monoclonal IgG antihuman A33-Alexa Fluor 488 (Clone # 402104) (R&D Systems, Minneapolis, MN), 15 and a monoclonal IgG antihuman-CD45-APC, a marker of all leukocyte groups (BD Pharmingen, San Jose, CA). Appropriate isotype controls were included (IgG2a-Alexa Fluor 488 (R&D Systems) and IgG1-APC, (BD Pharmingen)) as described 16 and analyzed by flow cytometry in a FACS CANTO II (Becton-Dikinson Biosciences, San Jose, CA, USA).…”