Detection of Syndecan‑1/CD138 in T1165 Mouse Cell Line by Flow Cytometry.
T1165 mouse plasmacytoma cell line cultured with 10 ng/mL Recombinant Human IL‑6 (Catalog # 206-IL) was stained with 0.5 μg Rat Anti-Mouse Syndecan‑1/CD138 Alexa Fluor® 488‑conjugated Monoclonal Antibody (Catalog # FAB2966G, filled histogram) or isotype control antibody (Catalog # IC005G, open histogram). View our protocol for Staining Membrane-associated Proteins.
Preparation and Storage
The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.
Stability & Storage
Protect from light. Do not freeze.
12 months from date of receipt, 2 to 8 °C as supplied.
Syndecan-1, designated CD138, is a dimeric type I transmembrane (TM) protein that belongs to the Syndecan family of Type 1 transmembrane proteins (1, 2). The four Syndecan family members are major carriers of heparan sulfate (HS) and chondroitin sulfate glycosaminoglycans (GAGs) that have different expression patterns and extracellular sequences. Syndecan-1 forms weak non-covalent homodimers, or heterodimers with Syndecan-2 or -3, through interactions of the transmembrane domain (3). It is synthesized as a 310 amino acid (aa) precursor with a 22 aa signal sequence, a 233 aa extracellular domain (ECD) that includes three closely spaced consensus Ser-Gly HS attachment sites near the N-terminus, a 21 aa TM segment, and a 35 aa cytoplasmic region that includes a PDZ binding motif with a tyrosine phosphorylation site (4). The ECD is variably modified by GAGs, producing molecular weights of 120‑200 kDa for native Syndecan-1. Soluble forms are shed via proteolytic cleavage. Mouse Syndecan-1 ECD shares 70% and 87% aa identity with the ECD of human and rat Syndecan-1, respectively. Alternative splicing in mouse generates an isoform with an internal deletion of 44 aa from the ECD (5). Syndecan-1 shows highest expression on epithelial cells such as keratinocytes, and terminally differentiated B cells such as plasma cells (6, 7). It aids wound healing in skin, cornea, and heart following myocardial infarction by promoting re-epithelialization, migration, and collagen deposition (6‑10). It binds chemokines, creating chemotactic gradients when shed, but also binds and modulates integrins to control the influx of leukocytes (7, 9, 11). The net effect is to allow, but limit, inflammation. In myeloma and other cancers, shedding of Syndecan-1 can facilitate growth, angiogenesis and metastasis (12‑14). Growth factors, such as FGFs and HGF, bind GAG chains and use Syndecan-1 as a coreceptor (14, 15). The GAG chains may also be used by a variety of viruses and bacteria for cell adhesion and uptake (6).
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