--Mark Hill 07:47, 29 March 2009 (EST) Thank you for your feedback. Lecture 4 - Cell Nucleus did not discuss cell adhesion, so I find you comment a little confusing. Have a look at the nucleus information again. Cell Export - Exocytosis I am glad you found the content easy to understand and to listen too. Yes, the unique nuclear lamin skeleton will be discussed in Cytoskeleton - Intermediate Filaments and Cell Division.
Tumor Necrosis Factor (TNF) Individual Project - Cell Biology
OMIM Resource: http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=191160
What is TNF? Structure Function: main and specific, esp. in inducing apoptosis. Signaling (inc. 2 receptors for TNF - TNFR1, TNFR2) TNF and its role in Apoptotic Cell Death: Abnormalities: Significance (of research): Future Research:
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta ( LYMPHOTOXIN), but they share TNF RECEPTORS.
http://www.genecards.org/cgi-bin/carddisp.pl?gene=TNF This gene encodes a multifunctional proinflammatory cytokine that belongs to the tumor necrosis factor (TNF) superfamily. This cytokine is mainly secreted by macrophages. It can bind to, and thus functions through its receptors TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR. This cytokine is involved in the regulation of a wide spectrum of biological processes including cell proliferation, differentiation, apoptosis, lipid metabolism, and coagulation. This cytokine has been implicated in a variety of diseases, including autoimmune diseases, insulin resistance, and cancer. Knockout studies in mice also suggested the neuroprotective function of this cytokine. [provided by RefSeq] UniProtKB/Swiss-Prot: TNFA_HUMAN, P01375 Function: Cytokine that binds to TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR. It is mainly secreted by macrophages and can induce cell death of certain tumor cell lines. It is potent pyrogen causing fever by direct action or by stimulation of interleukin-1 secretion and is implicated in the induction of cachexia, Under certain conditions it can stimulate cell proliferation and induce cell differentiation. http://www.ncbi.nlm.nih.gov/pubmed/10634209: Out of the almost 17 members of the TNF superfamily, TNF is probably the most potent inducer of apoptosis. TNF activates both cell-survival and cell-death mechanisms simultaneously. Activation of NF-kB-dependent genes regulates the survival and proliferative effects pf TNF, whereas activation of caspases regulates the apoptotic effects. TNF-induced apoptosis is mediated primarily through the activation of type I receptors, the death domain of which recruits more than a dozen different signaling proteins, which together are considered part of an apoptotic cascade. This cascade does not, however, account for the role of reactive oxygen intermediates, ceramide, phospholipases, and serine proteases which are also implicated in TNF-induced apoptosis. This cascade also does not explain how type II TNF receptors which lack the death domain, induce apoptosis. Nevertheless, this review of apoptosis signaling will be limited to those proteins that makeup the cascade. http://www.ncbi.nlm.nih.gov/pubmed/11431320:Good for mutation stuff – mutations inhibit apoptosis and induce metastasis in breast cancer. TNF – Individual Project for Cell Biology
Pubmed abstract on TNF-induced apoptosis http://www.ncbi.nlm.nih.gov/pubmed/10634209
Mediation of TNF-induced Apoptosis by p38 http://www.ncbi.nlm.nih.gov/pubmed/15265709
Mitochondria in TNF-induced Apoptosis Good article/research paper: http://www.genebee.msu.su/cmm/skulach.html