TNF receptor superfamily member 13B

mammalian protein found in Homo sapiens
Protein protein Q21119508
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TNF receptor superfamily member 13B

Summary

TNF receptor superfamily member 13B is a protein[1].

Key Facts

  • TNF receptor superfamily member 13B's instance of is recorded as protein[2].
  • TNF receptor superfamily member 13B's UniProt protein ID is recorded as O14836[3].
  • TNF receptor superfamily member 13B's part of is recorded as Tumour necrosis factor receptor 13B[4].
  • TNF receptor superfamily member 13B's part of is recorded as TACI, cysteine-rich domain, protein family[5].
  • TNF receptor superfamily member 13B's MeSH descriptor ID is recorded as D053303[6].
  • TNF receptor superfamily member 13B's has part is recorded as TACI, cysteine-rich domain[7].
  • TNF receptor superfamily member 13B's RefSeq protein ID is recorded as NP_036584[8].
  • TNF receptor superfamily member 13B's PDB structure ID is recorded as 1XU1[9].
  • TNF receptor superfamily member 13B's PDB structure ID is recorded as 1XUT[10].
  • TNF receptor superfamily member 13B's MeSH tree code is recorded as D12.776.543.750.705.852.760.899[11].
  • TNF receptor superfamily member 13B's molecular function is recorded as protein binding[12].
  • TNF receptor superfamily member 13B's molecular function is recorded as signaling receptor activity[13].
  • TNF receptor superfamily member 13B's cell component is recorded as integral component of membrane[14].
  • TNF receptor superfamily member 13B's cell component is recorded as integral component of plasma membrane[15].
  • TNF receptor superfamily member 13B's cell component is recorded as membrane[16].
  • TNF receptor superfamily member 13B's cell component is recorded as plasma membrane[17].
  • TNF receptor superfamily member 13B's cell component is recorded as plasma membrane[18].
  • TNF receptor superfamily member 13B's biological process is recorded as cell surface receptor signaling pathway[19].
  • TNF receptor superfamily member 13B's biological process is recorded as tumor necrosis factor-mediated signaling pathway[20].
  • TNF receptor superfamily member 13B's biological process is recorded as adaptive immune response[21].
  • TNF receptor superfamily member 13B's biological process is recorded as immune system process[22].
  • TNF receptor superfamily member 13B's biological process is recorded as B cell homeostasis[23].
  • TNF receptor superfamily member 13B's biological process is recorded as hematopoietic progenitor cell differentiation[24].
  • TNF receptor superfamily member 13B's biological process is recorded as negative regulation of B cell proliferation[25].
  • TNF receptor superfamily member 13B's encoded by is recorded as TNFRSF13B[26].

References

Programmatic citations — every numbered marker resolves to a verifiable graph row below.

Direct Wikidata claims

  1. [2] . Q905695. Retrieved . wikidata.org.
  2. [3] . Q905695. Retrieved . wikidata.org.
  3. [4] . InterPro Release 71.0. ebi.ac.uk. Provenance: wikidata.org.
  4. [5] . wikidata.org.
  5. [6] . wikidata.org.
  6. [7] . InterPro Release 71.0. ebi.ac.uk. Provenance: wikidata.org.
  7. [8] . Q20641742. Retrieved . wikidata.org.
  8. [9] . Q905695. Retrieved . wikidata.org.
  9. [10] . Q905695. Retrieved . wikidata.org.
  10. [11] . wikidata.org.
  11. [12] . The transmembrane activator TACI triggers immunoglobulin class switching by activating B cells through the adaptor MyD88. Retrieved . ebi.ac.uk. Provenance: wikidata.org.
  12. [13] . NF-AT Activation Induced by a CAML-Interacting Member of the Tumor Necrosis Factor Receptor Superfamily. Retrieved . ebi.ac.uk. Provenance: wikidata.org.
  13. [14] . GOA. Retrieved . ebi.ac.uk. Provenance: wikidata.org.
  14. [15] . NF-AT Activation Induced by a CAML-Interacting Member of the Tumor Necrosis Factor Receptor Superfamily. Retrieved . ebi.ac.uk. Provenance: wikidata.org.
  15. [16] . GOA. Retrieved . ebi.ac.uk. Provenance: wikidata.org.
  16. [17] . GOA. Retrieved . ebi.ac.uk. Provenance: wikidata.org.
  17. [18] . GOA. Retrieved . ebi.ac.uk. Provenance: wikidata.org.
  18. [19] . NF-AT Activation Induced by a CAML-Interacting Member of the Tumor Necrosis Factor Receptor Superfamily. Retrieved . ebi.ac.uk. Provenance: wikidata.org.
  19. [20] . GOA. Retrieved . ebi.ac.uk. Provenance: wikidata.org.
  20. [21] . GOA. Retrieved . ebi.ac.uk. Provenance: wikidata.org.
  21. [22] . GOA. Retrieved . ebi.ac.uk. Provenance: wikidata.org.
  22. [23] . Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Retrieved . ebi.ac.uk. Provenance: wikidata.org.
  23. [24] . Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Retrieved . ebi.ac.uk. Provenance: wikidata.org.
  24. [25] . Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Retrieved . ebi.ac.uk. Provenance: wikidata.org.
  25. [26] . Q905695. Retrieved . wikidata.org.

Class ancestry

  1. [1] . Wikidata. wikidata.org.

📑 Cite this page

Use these citations when quoting this entity in research, articles, AI prompts, or wherever provenance matters. We aggregate Wikidata + Wikipedia + authoritative open-data sources; the stitched, scored, cross-referenced view is what 4ort.xyz contributes.

APA 4ort.xyz Knowledge Graph. (2026). TNF receptor superfamily member 13B. Retrieved May 3, 2026, from https://4ort.xyz/entity/tnf-receptor-superfamily-member-13b
MLA “TNF receptor superfamily member 13B.” 4ort.xyz Knowledge Graph, 4ort.xyz, 3 May. 2026, https://4ort.xyz/entity/tnf-receptor-superfamily-member-13b.
BibTeX @misc{4ortxyz_tnf-receptor-superfamily-member-13b_2026, author = {{4ort.xyz Knowledge Graph}}, title = {{TNF receptor superfamily member 13B}}, year = {2026}, url = {https://4ort.xyz/entity/tnf-receptor-superfamily-member-13b}, note = {Accessed: 2026-05-03}}
LLM prompt According to 4ort.xyz Knowledge Graph (aggregator of Wikidata, Wikipedia, and authoritative open-data sources): TNF receptor superfamily member 13B — https://4ort.xyz/entity/tnf-receptor-superfamily-member-13b (retrieved 2026-05-03)

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