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Disease relevance of Apoptosis


Psychiatry related information on Apoptosis


High impact information on Apoptosis

  • T cell apoptosis occurs in at least two major forms: antigen-driven and lymphokine withdrawal [11].
  • Positive selection refers to the active process of rescuing MHC-restricted thymocytes from programmed cell death [12].
  • An expanding family of BCL-2 related proteins share homology, clustered within four conserved regions, namely BCL-2 homology (BH1-4) domains, which control the ability of these proteins to dimerize and function as regulators of apoptosis [13].
  • The pre-T cell receptor (pre-TCR) that minimally consists of the TCR beta chain and the disulfide-linked pre-T cell receptor alpha (pT alpha) chain in association with signal-transducing CD3 molecules rescues from programmed cell death cells with productive TCR beta rearrangements [14].
  • Extracellularly, TRX/ADF shows a cytoprotective activity against oxidative stress-induced apoptosis and a growth-promoting effect as an autocrine growth factor [15].

Chemical compound and disease context of Apoptosis


Biological context of Apoptosis

  • Certain structural features of PTEN contribute to its specificity for PIP3, as well as its role(s) in regulating cellular proliferation and apoptosis [1].
  • Recent studies have demonstrated that PTEN plays an essential role in regulating signaling pathways involved in cell growth and apoptosis, and mutations in the PTEN gene are now known to cause tumorigenesis in a number of human tissues [1].
  • The mutant Trp53 was abundant, its level was not affected by DNA damage and it bound DNA constitutively; however, it showed defects in cell-cycle regulation and apoptosis [21].
  • The gene egl-1 encodes a BH3-containing cell death activator that is required for programmed cell death in C. elegans [22].
  • Both natural and recombinant TIA-1 were found to induce DNA fragmentation in digitonin permeabilized thymocytes, suggesting that these molecules may be the granule components responsible for inducing apoptosis in CTL targets [23].

Anatomical context of Apoptosis


Associations of Apoptosis with chemical compounds

  • The PTP superfamily enzymes, which include tyrosine-specific, dual specificity, low-molecular-weight, and Cdc25 phosphatases, are key mediators of a wide variety of cellular processes, including growth, metabolism, differentiation, motility, and programmed cell death [1].
  • All apoptosis signaling pathways converge on a common machinery of cell destruction that is activated by a family of cysteine proteases (caspases) that cleave proteins at aspartate residues [29].
  • We also found that Pml is essential for induction of programmed cell death by Fas, tumour necrosis factor alpha (TNF), ceramide and type I and II interferons (IFNs) [30].
  • Casp9-/- thymocytes are also resistant to dexamethasone- and gamma irradiation-induced apoptosis, but are surprisingly sensitive to apoptosis induced by UV irradiation or anti-CD95 [31].
  • Caspases are cysteine proteases that mediate programmed cell death in phylogenetically diverse multicellular organisms [32].

Gene context of Apoptosis

  • The onset of apoptosis can be delayed by cross-linking centrocytes' surface Ig, and long-term survival is achieved by signalling through their surface CD40 [33].
  • Disruption of p73 function by a tumour-derived p53 mutant reduced E2F1-mediated apoptosis [34].
  • Overexpression of Daxx enhances Fas-mediated apoptosis and activates the Jun N-terminal kinase (JNK) pathway [35].
  • Heterozygous mutation of Trp53 decreases p53 and results in attenuated apoptosis and G1-S checkpoint control, allowing Brca1Delta11/Delta11 cells to proliferate [36].
  • In vitro, this mutation was associated with an inability of IB1 to prevent apoptosis induced by MAPK/ERK kinase kinase 1 (MEKK1) and a reduced ability to counteract the inhibitory action of the activated c-JUN amino-terminal kinase (JNK) pathway on INS transcriptional activity [37].

Analytical, diagnostic and therapeutic context of Apoptosis

  • Ligation of JAM is required for reovirus-induced activation of NF-kappaB and apoptosis [38].
  • Orthotopically grown tumors and low-density cell cultures derived from antisense caveolin clones had increased apoptosis in the absence of androgenic steroids, whereas similarly grown tumors and cells from vector (control) clones and parental cells were not sensitive to androgens [39].
  • In contrast, treatment with cyclosporine A and co-stimulation blockade abolished T-cell proliferation and apoptosis, as well as the induction of stable allograft tolerance [40].
  • Previously, we cloned a cDNA fragment, TSIP 2 (tumor suppressor inhibited pathway clone 2), that detects by northern blot analysis of M1-LTR6 cells a 3-kb mRNA downregulated during p53-induced apoptosis [41].
  • We used the TUNEL technique to assay DNA degradation in nuc-1 and other mutants defective in programmed cell death and discovered that TUNEL labels apoptotic cells only during a transient intermediate stage [42].


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  15. Redox regulation of cellular activation. Nakamura, H., Nakamura, K., Yodoi, J. Annu. Rev. Immunol. (1997) [Pubmed]
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  18. Ferredoxin reductase affects p53-dependent, 5-fluorouracil-induced apoptosis in colorectal cancer cells. Hwang, P.M., Bunz, F., Yu, J., Rago, C., Chan, T.A., Murphy, M.P., Kelso, G.F., Smith, R.A., Kinzler, K.W., Vogelstein, B. Nat. Med. (2001) [Pubmed]
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