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APRIL (protein)

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(Redirected fromTNFSF13)

TNFSF13
Available structures
PDBOrtholog search:PDBeRCSB
Identifiers
AliasesTNFSF13,APRIL, CD256, TALL-2, TALL2, TRDL-1, ZTNF2, UNQ383/PRO715, TNLG7B, tumor necrosis factor superfamily member 13, TNF superfamily member 13
External IDsOMIM:604472;MGI:1916833;HomoloGene:56971;GeneCards:TNFSF13;OMA:TNFSF13 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001159505
NM_023517

RefSeq (protein)

NP_001152977
NP_076006

Location (UCSC)Chr 17: 7.56 – 7.56 MbChr 11: 69.57 – 69.58 Mb
PubMedsearch[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

A proliferation-inducing ligand(APRIL), also known astumor necrosis factor ligand superfamily member 13(TNFSF13), is aproteinof theTNFsuperfamily recognized by thecell surface receptorTACI.[5][6]It is encoded by theTNFSF13gene.[6]

Nomenclature

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In thecluster of differentiationterminology, APRIL is designatedCD256.

Function

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The protein encoded by this gene is a member of thetumor necrosis factorligand (TNF) ligand family. This protein is a ligand forTNFRSF17/BCMA, a member of theTNF receptorfamily. This protein and its receptor are both found to be important forB celldevelopment. In vivo experiments suggest an important role for APRIL in the long-term survival of plasma cells in the bone marrow. Mice deficient in APRIL have normal immune system development.[7]However, APRIL-deficient mice have also been reported to possess a reduced ability to support plasma cell survival.[8]In vitro experiments suggested that this protein may be able to induceapoptosisthrough its interaction with other TNF receptor family proteins such asTNFRSF6/FAS andTNFRSF14/HVEM.[9]Three alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported.

Interactions

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TNFSF13 has been shown tointeractwithTNFRSF13B[10]andB-cell activating factor.[11]

Clinical significance

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APRIL is being explored as a target for autoimmune diseases and B cell malignancies.[12]At least one anti-APRIL monoclonal antibody has been announced to enter phase I clinical trials formultiple myeloma.[13]

References

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  1. ^abcGRCh38: Ensembl release 89: ENSG00000161955Ensembl,May 2017
  2. ^abcGRCm38: Ensembl release 89: ENSMUSG00000089669Ensembl,May 2017
  3. ^"Human PubMed Reference:".National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^"Mouse PubMed Reference:".National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^Hahne M, Kataoka T, Schröter M, Hofmann K, Irmler M, Bodmer JL, et al. (September 1998)."APRIL, a new ligand of the tumor necrosis factor family, stimulates tumor cell growth".The Journal of Experimental Medicine.188(6): 1185–1190.doi:10.1084/jem.188.6.1185.PMC2212534.PMID9743536.
  6. ^ab"Entrez Gene: TNFSF13 tumor necrosis factor (ligand) superfamily, member 13".National Library of Medicine. 10 October 2023.Retrieved13 October2023.
  7. ^Varfolomeev E, Kischkel F, Martin F, Seshasayee D, Wang H, Lawrence D, et al. (February 2004)."APRIL-deficient mice have normal immune system development".Molecular and Cellular Biology.24(3): 997–1006.doi:10.1128/MCB.24.3.997-1006.2004.PMC321448.PMID14729948.
  8. ^Belnoue E, Pihlgren M, McGaha TL, Tougne C, Rochat AF, Bossen C, et al. (March 2008)."APRIL is critical for plasmablast survival in the bone marrow and poorly expressed by early-life bone marrow stromal cells".Blood.111(5): 2755–2764.doi:10.1182/blood-2007-09-110858.PMID18180376.
  9. ^Roth W, Wagenknecht B, Klumpp A, Naumann U, Hahne M, Tschopp J, et al. (April 2001)."APRIL, a new member of the tumor necrosis factor family, modulates death ligand-induced apoptosis".Cell Death and Differentiation.8(4): 403–410.doi:10.1038/sj.cdd.4400827.PMID11550092.
  10. ^Wu Y, Bressette D, Carrell JA, Kaufman T, Feng P, Taylor K, et al. (November 2000)."Tumor necrosis factor (TNF) receptor superfamily member TACI is a high affinity receptor for TNF family members APRIL and BLyS".The Journal of Biological Chemistry.275(45): 35478–35485.doi:10.1074/jbc.M005224200.PMID10956646.
  11. ^Roschke V, Sosnovtseva S, Ward CD, Hong JS, Smith R, Albert V, et al. (October 2002)."BLyS and APRIL form biologically active heterotrimers that are expressed in patients with systemic immune-based rheumatic diseases".Journal of Immunology.169(8): 4314–4321.doi:10.4049/jimmunol.169.8.4314.PMID12370363.
  12. ^Ryan MC, Grewal IS (2009-01-01). "Targeting of BAFF and APRIL for Autoimmunity and Oncology". In Grewal IS (ed.).Therapeutic Targets of the TNF Superfamily.Advances in Experimental Medicine and Biology. Vol. 647. New York: Springer. pp. 52–63.doi:10.1007/978-0-387-89520-8_4.ISBN978-0-387-89519-2.PMID19760066.
  13. ^"Development of a first in class APRIL fully blocking antibody BION-1301 for the treatment of multiple myeloma".AACR 2017 Proceedings.April 2017.

Further reading

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This article incorporates text from theUnited States National Library of Medicine,which is in thepublic domain.