APRIL, a member of the TNF superfamily, is expressed in monocytes, macrophages, certain transformed cell lines, certain cancers of the colon, and lymphoid tissues. APRIL, along with another TNF family member, BAFF, competes for two receptors, TACI and BCMA. APRIL has the ability to stimulate proliferation of various tumor cell lines, including Jurkat T cells and MCF-7 carcinoma cells. Like BAFF, APRIL also stimulates the proliferation of B and T cells. The human APRIL gene codes for at least four alternatively spliced transcriptional variants, which give rise to different isoforms of the APRIL precursor protein. All isoforms can be cleaved by the protease, furin, to release a soluble C-terminal fragment, which comprises the TNF-like receptor binding of the APRIL precursor. Recombinant human APRIL is a soluble 16.3 kDa protein, consisting of 146 amino acid residues.
Amino Acid Sequence
Hi-5 Insect cells
Measured by its ability to induce cell death in Jurkat cells.
Apoptosis, Autoimmunity, Cytokines and chemokines and related molecules, Immunology, Oncology
APRIL (A PRoliferation-Inducing Ligand) is a member of the tumor necrosis factor family. APRIL shows high levels of expression in tumors of different origin and low level of expression in normal cells. APRIL shares two TNF receptor family members, TACI and BCMA with another TNF homolog, BlyS/BAFF both of which have been reported to play a role in autoimmune disease and cancer. The gene encoding the APRIL protein is localized to chromosome 17g 13.3. APRIL appears to play a role in T-independent type II antigen responses and T cell survival, but can also induce proliferation/survival of non-lymphoid cells. Local production of APRIL was found in arthritic joints of patients with inflammatory arthritis. Biologically active BlyS/BAFF and APRIL heterotrimers are expressed in patients with systemic immune-based rheumatic diseases. A soluble form of the high affinity BCMA receptor has been shown to inhibit the proliferative activity of APRIL in vitro, thus decreasing tumor cell proliferation, while APRIL-transfected cells show an increased rate of tumor growth very directly, suggesting that APRIL is implicated in the regulation of tumor cell growth.