anti-PIDD (PIDD) Antikörper

Mouse (Murine) P53-Induced Death Domain Protein (PIDD) Interaktionspartner

1. NPM1 (zeige GJA1 Antikörper)-dependent nucleolar PIDDosome is a key initiator of the caspase-2 (zeige CASP2 Antikörper) activation cascade.

2. PIDD acts as a critical switcher between the NF-kappabeta (zeige NFKB1 Antikörper) transcription pathway and radiation-induced apoptosis

3. The tumor-modulatory effects of Caspase-2 (zeige CASP2 Antikörper) and Pidd1 do not require the scaffold protein (zeige HOMER1 Antikörper) Raidd (zeige CRADD Antikörper)

4. Loss of PIDD leads to an impaired inflammatory response after DNA damage.

5. Caspase 2 (zeige CASP2 Antikörper) activity can be induced in neurons from PIDD-null mice, and NGF (zeige NGFB Antikörper) deprivation or Abeta (zeige APP Antikörper) use caspase 2 (zeige CASP2 Antikörper) and RAIDD (zeige CRADD Antikörper) to execute death of these neurons.

6. P450 (zeige POR Antikörper) levels were higher in female DES (zeige DES Antikörper)-treated p53 (zeige TP53 Antikörper)+/- mice compared to treated wild type mice.

7. Results suggest that at least one alternative PIDDosome-independent mechanism of caspase-2 (zeige CASP2 Antikörper) activation exists in mammals in response to DNA damage.

8. PIDD does not play an essential role for all p53 (zeige TP53 Antikörper)-mediated or p53 (zeige TP53 Antikörper)-independent apoptotic pathways.

Human P53-Induced Death Domain Protein (PIDD) Interaktionspartner

1. Whole exome sequencing (WES) of an affected fetus, and subsequent Sanger sequencing of the second fetus, revealed a homozygous frameshift variant in CRADD (zeige CRADD Antikörper), which encodes an adaptor protein that interacts with PIDD and caspase-2 (zeige CASP2 Antikörper) to initiate apoptosis

2. NPM1 (zeige NPM1 Antikörper)-dependent nucleolar PIDDosome is a key initiator of the caspase-2 (zeige CASP2 Antikörper) activation cascade.

3. PIDD expression was lower in HCC (zeige FAM126A Antikörper) tissues and HCC (zeige FAM126A Antikörper) 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 (zeige FAM126A Antikörper) 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.

4. By sequestering PIDD at the kinetochore, BubR1 (zeige BUB1B Antikörper) acts to delay PIDDosome formation until the next cycle, defining a new mechanism by which cells evade apoptosis during mitosis.

5. The ATM (zeige ATM Antikörper) phosphorylation of the PIDD DD enables a binary switch through which cells elect to survive or die upon DNA injury.

6. PIDD performs key functions upon UV irradiation, including TLS (zeige FUS Antikörper), NHEJ, NF-kappaB (zeige NFKB1 Antikörper) activation and cell death.

7. Hsp90 (zeige HSP90 Antikörper) has a major role in controlling PIDD functional activity.

8. a new splicing variant of PIDD named PIDD4 is reported.

9. point mutations on RAIDD (zeige CRADD Antikörper) (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

10. Total caspase-2 (zeige CASP2 Antikörper) is upregulated during tumour progression in renal cell carcinomas.