Talk:TNF receptor superfamily

Untitled

This page is terribly full of errors. Take the gene names and go to pubmed OMIM.

I will help get you started.

TNFRSF1A " MIM ID *191190 TUMOR NECROSIS FACTOR RECEPTOR SUPERFAMILY, MEMBER 1A; TNFRSF1A

• TUMOR NECROSIS FACTOR RECEPTOR 1; TNFR1
• TUMOR NECROSIS FACTOR-ALPHA RECEPTOR; TNFAR
• TNFR, 55-KD
• TNFR, 60-KD

" NAME: TNFR1 LOCUS:TNFRSF1A

MIM ID *600315 TUMOR NECROSIS FACTOR RECEPTOR SUPERFAMILY, MEMBER 4; TNFRSF4

Alternative titles; symbols

• TAX-TRANSCRIPTIONALLY ACTIVATED GLYCOPROTEIN 1 RECEPTOR; TXGP1L
• OX40 ANTIGEN
• LYMPHOID ACTIVATION ANTIGEN ACT35; ACT35
• CD134

NAME: OX40 ALIAS:CD134, ACT35 LOCUS:TNFRSF4

Other forms of errors:

"Because "TNF" is often used to describe TNF alpha, "TNFR" is often used to describe the receptors that bind to TNF alpha - namely, CD120" = Nonsense.

The title should be Tumor Necrosis Factor Receptor Superfamily or Tumor Necrosis Factor Receptor Family. There are two TNF receptors by Name TNFR1 and TNFR2, the second has two isoforms, alpha and beta.

Tumor necrosis factor receptor superfamily (TNFRSF) are a group of receptors that bind members of the tumor necrosis factor superfamily of ligands. These ligands can either be cell surface bound or free. In addition the receptors are generally class II membrane proteins, but some are cleaved at the extracellular side of the plasma membrane creating free receptor which can take on other regulator functions. Many members of the TNFRSF family (e.g. TNFR1, Fas) are notable because of their promotion, regulation or inhibition of apoptosis. The apoptosis promotors act via intracellular signalling because of death-domain regions on their cytoplasmic tails. These death domain interact with death domains of cytosolic proteins like TRADD and FADD which then interact with effector molecules like pro-Caspase-8 which then activate Caspase-3 and leads to the disentregration of intracellular components. This cell killing "necrosis" activity is how the TNF and their receptors were recognized. Using comparative sequence analysis of ligands and receptors, other members of both superfamilies have since been recognized.

Certain TNFRSF have distinct immune activities such as CD40, OX40, CD30, CD70 independent of tumor necrosis and provide a wide variety of stimulatory and regulatory functions. CD40 appears to play a critical role in B-cell maturation and activity. Like TNF-R1, CD30, can stimulate NFkB activation, and the protein plays a role in B- and T-cell activation. OX40 is involved in immune tolerance induction. Other receptors are involved in bone growth, fat metabolism, etc.

Overexpression or underexpression of TNFSFR, their cognate ligands or downstream effortors are a cause of immunological and malignant disease. For example missense mutations in TNFRSF1A cause TRAPs which causes localized autoimmunity. Overexpression of CD40 ligand as a consequence of female inactive-X demethylation is associated with more severe forms of lupus (SLE). Loss of function mutations in TNFRSF4 gene (Fas gene) are known cause autoimmune lymphoproliferative syndrome. Somatic mutations within TNFSFR4 are often found in malignant tissues such as burn-scar related squamous cell carcinoma and lung cancers.

You folks can work out the details. My point here is, if it isn't a fact, it does not belong here. If its false, or terribly obsolete, it does not belong here.

Also please pay attention to the pages that are being pointed to some show little consistency with this page. The gene names appear to be correct, search the alias and you can see which is most commonly used. In the example above

CD120 is mentioned in 4 papers (2 of which were in english with one russian authorship with meaning of CD120 unclear). TNFR1 or TNF-R1 are mentioned in around 3800 papers TNFRSF1A is mentioned in around 330 papers.

For TNFRSF4: OX40 - 705 publications CD134 - 234 publications TNFRSF4 - 432 (Again those that do not mention OX40[many] or CD134 may be talking about gene associations)

One should strive to use the nomenclature most commonly used in the scientific literature make it easier for readers to use this media as a launch point for more in-depth research. The names should reflect the names most commonly encountered in the current literature and should avoid names that might be used for something else. PB666 ^yap 04:20, 30 April 2011 (UTC)