Category: Proteins & Peptides

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Reference: GTX27865

Survivin, a new inhibitor of apoptosis (IAP) protein, is expressed in the G2 / M phase of the cell cycle in a cycle regulated manner. At the beginning of mitosis, survivin associates with microtubules of the mitotic spindle in a specific and saturable reaction that is regulated by microtubule dynamics. Disruption of survivin microtubule interactions results in loss of survivin's anti apoptosis function and increased caspase 3 activity, a mechanism involved in cell death, during mitosis. It indicates that survivin may counteract a default induction of apoptosis in G2 / M phase. The over expression of survivin in cancer may overcome this apoptotic checkpoint and favour aberrant progression of transformed cells through mitosis.

Reference: GTX27866

Survivin, a new inhibitor of apoptosis (IAP) protein, is expressed in the G2 / M phase of the cell cycle in a cycle regulated manner. At the beginning of mitosis, survivin associates with microtubules of the mitotic spindle in a specific and saturable reaction that is regulated by microtubule dynamics. Disruption of survivin microtubule interactions results in loss of survivin's anti apoptosis function and increased caspase 3 activity, a mechanism involved in cell death, during mitosis. It indicates that survivin may counteract a default induction of apoptosis in G2 / M phase. The over expression of survivin in cancer may overcome this apoptotic checkpoint and favour aberrant progression of transformed cells through mitosis.

Reference: GTX27867

Apoptosis or programmed cell death is induced in cells by a group of death domain containing receptors. Binding of ligand to these receptors sends signals that activate members of the caspase family of proteases. The signals ultimately cause degradation of chromosomal DNA by activating DNase. TRAIL (TNF related apoptosis induced ligand) or Apo 2L initiates apoptosis of tumor cells by binding to either of its receptors, DR4 or DR5. These receptors consist of an extracellular TRAIL binding domain and a cytoplasmic ""death domain"". In addition, two decoy receptors for TRAIL have also been identified. These receptors, designated DcR1 and DcR2, lack the death domain. Binding of TRAIL to either of these receptors, therefore, does not transmit the death signal. Thus, these receptors represent a novel way of regulating cell sensitivity to a pro-apoptotic cytokine at the cell surface. TRAIL is expressed predominantly in spleen, lung, and prostate but also in many other tissues.

Reference: GTX27868

Proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) contributes to a variety of inflammatory responses and programmed cell death. Notch receptor and its ligand participate in cell fate decisions during vertebrate development and are associated with several human disorders, including a T-cell lymphoma. TNF-alpha, Notch and its ligand Delta are all membrane bound molecules, which are cleaved by proteases. ADAM1, a metalloprotease-disintegrin from the family of mammalian ADAMs (a disintegrin and metalloprotease), cleaves amyloid plaque protein, TNF-alpha, Notch, and its ligand Delta. ADAM1 contains the canonical HExxHxxxxxH zinc metalloproteinase motif. In bovine kidney, ADAM1 cleaves Type IV collagen. ADAM1 is efficiently inhibited by the endogenous MMP inhibitors TIMP1 and TIMP3, but not by TIMP2 and TIMP4. ADAM1 is widely expressed in tissues and can be found on the cell surface and within the cell. The genes encoding human, mouse and bovine ADAM1 are designated ADAM1, kuzbanian (KUZ), and MADM respectively and have 97% sequence identity with each other and with rat ADAM1. There is 45% identity between mouse and Drosophila.

Reference: GTX27869

This gene encodes a flavoprotein essential for nuclear disassembly in apoptotic cells, and it is found in the mitochondrial intermembrane space in healthy cells. Induction of apoptosis results in the translocation of this protein to the nucleus where it affects chromosome condensation and fragmentation. In addition, this gene product induces mitochondria to release the apoptogenic proteins cytochrome c and caspase-9. Mutations in this gene cause combined oxidative phosphorylation deficiency 6 (COXPD6), a severe mitochondrial encephalomyopathy, as well as Cowchock syndrome, also known as X-linked recessive Charcot-Marie-Tooth disease-4 (CMTX-4), a disorder resulting in neuropathy, and axonal and motor-sensory defects with deafness and cognitive disability. Alternative splicing results in multiple transcript variants. A related pseudogene has been identified on chromosome 1. [provided by RefSeq, Aug 215]

Reference: GTX27870

This gene encodes a flavoprotein essential for nuclear disassembly in apoptotic cells, and it is found in the mitochondrial intermembrane space in healthy cells. Induction of apoptosis results in the translocation of this protein to the nucleus where it affects chromosome condensation and fragmentation. In addition, this gene product induces mitochondria to release the apoptogenic proteins cytochrome c and caspase-9. Mutations in this gene cause combined oxidative phosphorylation deficiency 6 (COXPD6), a severe mitochondrial encephalomyopathy, as well as Cowchock syndrome, also known as X-linked recessive Charcot-Marie-Tooth disease-4 (CMTX-4), a disorder resulting in neuropathy, and axonal and motor-sensory defects with deafness and cognitive disability. Alternative splicing results in multiple transcript variants. A related pseudogene has been identified on chromosome 1. [provided by RefSeq, Aug 215]