Apoptosis Reference Genome Targets (Archived): Difference between revisions

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[2] http://en.wikipedia.org/wiki/Apoptosis
[2] http://en.wikipedia.org/wiki/Apoptosis
[3] Molecular mechanisms of caspase regulation during apoptosis, Nature Reviews Molecular Cell Biology 5, 897-907 (November 2004) | doi:10.1038/nrm1496
[4] APOPTOSIS PATHWAYS AND DRUG TARGETS POSTER:
John C. Reed and Ziwei Huang: http://www.nature.com/reviews/poster/apoptosis/index.html


==Families to annotate (BATCH 1) ==
==Families to annotate (BATCH 1) ==


== Annotation targets/progress table (BATCH 1) ==
== Annotation targets/progress table (BATCH 1) ==

Revision as of 13:34, 28 February 2011

Project leaders

UniProtKB GOA team, Emily Dimmer

Justification (Impact and significance)

Apoptosis is the process of programmed cell death (PCD) that may occur in multicellular organisms.

Biochemical events lead to characteristic cell changes (morphology) and death. These changes include rounding-up of the cell, retraction of pseudopodes, plasma membrane blebbing, loss of cell membrane asymmetry and attachment,reduction of cellular volume (pyknosis), nuclear fragmentation (karyorrhexis), chromatin condensation, and chromosomal DNA fragmentation. Apoptosis produces cell fragments called apoptotic bodies that surrounding cells are able to engulf (often associated with phagocytes) and quickly remove before the contents of the cell can spill out onto surrounding cells and cause damage. Apoptosis is not synonymous with programmed cell death (PCD).

In addition to its importance as a biological phenomenon, defective apoptotic processes have been implicated in an extensive variety of diseases. Excessive apoptosis causes atrophy, such as in ischemic damage, whereas an insufficient amount results in uncontrolled cell proliferation, such as cancer. [1],[2]


Notes for curators

Although the presence of active caspases and DNA fragmentation is helpful in identifying possible apoptosis, they should not be employed as an exclusive means to demonstrate this process as apototic cell death can occur without th DNA fragmentation or caspase activity.[1]


Cell death is frequently considered to be ‘caspase-dependent’ when it is suppressed by broad-spectrum caspase inhibitors such as N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (Z-VAD-fmk). As a word of caution, however, it should be noted that Z-VAD-fmk does not act on all caspases with an equal efficiency, and it also inhibits calpains and cathepsins, especially at high concentrations (>10 μM). Moreover, Z-VAD-fmk has been associated with several off-target effects that would result from the binding to cysteines on proteins other than cysteine proteases[1]

Range of species in which the pathway is found

Apoptosis Experts

Ontology status

Time frame of the project

see also: http://wiki.geneontology.org/index.php/Apoptosis

Background reading

[1] [Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009. Kroemer G, Galluzzi L, Vandenabeele P, Abrams J, Alnemri ES, Baehrecke EH, Blagosklonny MV, El-Deiry WS, Golstein P, Green DR, Hengartner M, Knight RA, Kumar S, Lipton SA, Malorni W, Nuñez G, Peter ME, Tschopp J, Yuan J, Piacentini M, Zhivotovsky B, Melino G; Nomenclature Committee on Cell Death 2009.Cell Death Differ. 2009 Jan;16(1):3-11. Epub 2008 Oct 10. http://www.ncbi.nlm.nih.gov/pubmed/18846107]

Highly recommended to read before starting curation; contains definitions of different types of cell death (apoptosis/necrosis/autophagic cell death/cornification, as described by the Nomenclature Committee on Cell Death.

[2] http://en.wikipedia.org/wiki/Apoptosis

[3] Molecular mechanisms of caspase regulation during apoptosis, Nature Reviews Molecular Cell Biology 5, 897-907 (November 2004) | doi:10.1038/nrm1496

[4] APOPTOSIS PATHWAYS AND DRUG TARGETS POSTER: John C. Reed and Ziwei Huang: http://www.nature.com/reviews/poster/apoptosis/index.html

Families to annotate (BATCH 1)

Annotation targets/progress table (BATCH 1)