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Human Polyclonal PIDD Primary Antibody for IP, IHC - ABIN1169268
Tinel, Tschopp: The PIDDosome, a protein complex implicated in activation of caspase-2 in response to genotoxic stress. in Science (New York, N.Y.) 2004
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Human Monoclonal PIDD Primary Antibody for IHC, IHC (p) - ABIN4331451
Tinel, Janssens, Lippens, Cuenin, Logette, Jaccard, Quadroni, Tschopp: Autoproteolysis of PIDD marks the bifurcation between pro-death caspase-2 and pro-survival NF-kappaB pathway. in The EMBO journal 2007
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NPM1 (show GJA1 Antibodies)-dependent nucleolar PIDDosome is a key initiator of the caspase-2 (show CASP2 Antibodies) activation cascade.
PIDD acts as a critical switcher between the NF-kappabeta (show NFKB1 Antibodies) transcription pathway and radiation-induced apoptosis
The tumor-modulatory effects of Caspase-2 (show CASP2 Antibodies) and Pidd1 do not require the scaffold protein (show HOMER1 Antibodies) Raidd (show CRADD Antibodies)
Loss of PIDD leads to an impaired inflammatory response after DNA damage.
Caspase 2 (show CASP2 Antibodies) activity can be induced in neurons from PIDD-null mice, and NGF (show NGFB Antibodies) deprivation or Abeta (show APP Antibodies) use caspase 2 (show CASP2 Antibodies) and RAIDD (show CRADD Antibodies) to execute death of these neurons.
P450 (show POR Antibodies) levels were higher in female DES (show DES Antibodies)-treated p53 (show TP53 Antibodies)+/- mice compared to treated wild type mice.
Results suggest that at least one alternative PIDDosome-independent mechanism of caspase-2 (show CASP2 Antibodies) activation exists in mammals in response to DNA damage.
PIDD does not play an essential role for all p53 (show TP53 Antibodies)-mediated or p53 (show TP53 Antibodies)-independent apoptotic pathways.
Whole exome sequencing (WES) of an affected fetus, and subsequent Sanger sequencing of the second fetus, revealed a homozygous frameshift variant in CRADD (show CRADD Antibodies), which encodes an adaptor protein that interacts with PIDD and caspase-2 (show CASP2 Antibodies) to initiate apoptosis
NPM1 (show NPM1 Antibodies)-dependent nucleolar PIDDosome is a key initiator of the caspase-2 (show CASP2 Antibodies) activation cascade.
PIDD expression was lower in HCC (show FAM126A Antibodies) tissues and HCC (show FAM126A Antibodies) cell lines, compared with the adjacent non-tumorous tissues and LO2 normal hepatocytes. PIDD could serve as an independent prognostic factor to predict the survival of HCC (show FAM126A Antibodies) patients. PIDD facilitated cell cycle progression and accelerated cell proliferation in HepG2 cells, while overexpression of PIDD resulted in cell cycle arrest at G1 phase in Hep3B cells.
By sequestering PIDD at the kinetochore, BubR1 (show BUB1B Antibodies) acts to delay PIDDosome formation until the next cycle, defining a new mechanism by which cells evade apoptosis during mitosis.
The ATM (show ATM Antibodies) phosphorylation of the PIDD DD enables a binary switch through which cells elect to survive or die upon DNA injury.
PIDD performs key functions upon UV irradiation, including TLS (show FUS Antibodies), NHEJ, NF-kappaB (show NFKB1 Antibodies) activation and cell death.
Hsp90 (show HSP90 Antibodies) has a major role in controlling PIDD functional activity.
a new splicing variant of PIDD named PIDD4 is reported.
point mutations on RAIDD (show CRADD Antibodies) (R147E) and on PIDD (Y814A) exert a dominant negative effect on the formation of the PIDDosome, and that this effect cannot be applied after the PIDDosome has been formed
Total caspase-2 (show CASP2 Antibodies) is upregulated during tumour progression in renal cell carcinomas.
The protein encoded by this gene contains a leucine-rich repeat and a death domain. This protein has been shown to interact with other death domain proteins, such as Fas (TNFRSF6)-associated via death domain (FADD) and MAP-kinase activating death domain-containing protein (MADD), and thus may function as an adaptor protein in cell death-related signaling processes. The expression of the mouse counterpart of this gene has been found to be positively regulated by the tumor suppressor p53 and to induce cell apoptosis in response to DNA damage, which suggests a role for this gene as an effector of p53-dependent apoptosis. Alternative splicing results in multiple transcript variants.
leucine-rich repeat and death domain-containing protein
, p53 protein induced, with death domain
, p53-induced protein with a death domain
, leucine-rich repeats and death domain containing