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The authors find that primary human aggressive B-cell lymphoma samples exhibit high USP9X (show USP9X ELISA Kits) expression that correlate with XIAP overexpression.
Findings reveal important new insights into how XIAP 3'UTR (show UTS2R ELISA Kits) works, suggesting that the non-coding XIAP 3'UTR (show UTS2R ELISA Kits) serves as a competitor for miRNA binding and subsequently inactivates miRNA functions, by which XIAP 3'UTR (show UTS2R ELISA Kits) frees the target mRNAs from being repressed.
XIAP is stable during mitotic arrest, but its function is controlled through phosphorylation by the mitotic kinase CDK1 (show CDK1 ELISA Kits)-cyclin-B1 (show CCNB1 ELISA Kits) at S40.
our findings suggest that X-linked inhibitor of apoptosis protein 3'-untranslated region serves as a competitive endogenous RNA for HMGA2 to activate hepatocellular carcinoma progression by arresting endogenous let-7a-5p.
In chronic myeloid leukemia (show BCL11A ELISA Kits) cells, EZH2 (show EZH2 ELISA Kits) modulates epigenetic changes at DNA methylated regions encoding miR (show MLXIP ELISA Kits)-219 and downregulates the level of miR (show MLXIP ELISA Kits)-219. Downregulation of miR (show MLXIP ELISA Kits)-219 results in upregulation of XIAP and supports the survival of leukemia cells.
IFNgamma positively affects NOD2 (show NOD2 ELISA Kits)-mediated signaling in human conventional dendritic cells, in a manner considerably dependent on XIAP and partially dependent on mTOR (show FRAP1 ELISA Kits).
miR (show MLXIP ELISA Kits)-137 expression is inversely correlated with the level of XIAP protein in both ovarian cancer tissues and cell lines. these data suggest that multiple miRNAs can regulate XIAP via its 3'UTR (show UTS2R ELISA Kits). miR (show MLXIP ELISA Kits)-137 can sensitise ovarian cancer cells to cisplatin-induced apoptosis, providing new insight into overcoming drug resistance in ovarian cancer
results of this work support the role of XIAP in mediating NOD2 (show NOD2 ELISA Kits) signaling while reconciling the role of X-linked lymphoproliferative syndrome 2 and very-early-onset inflammatory bowel disease XIAP mutations in inflammatory cell death and provide a set of tools and framework to rapidly test newly discovered XIAP variants.
Using recombinant proteins, this study investigated the influence of survivin (show BIRC5 ELISA Kits) on the inhibition of caspase-9 (show CASP9 ELISA Kits) by XIAP in vitro. With a fluorescence-based assay for the apoptosome-stimulated activity of caspase-9 (show CASP9 ELISA Kits), the study shows that survivin (show BIRC5 ELISA Kits) has no effect on the inhibition of caspase-9 (show CASP9 ELISA Kits) by XIAP, neither in the presence nor in the absence of Smac (show DIABLO ELISA Kits).
Study found a negative correlation between Smac (show DIABLO ELISA Kits) and XIAP at the level of protein but not mRNA in non-small cell lung carcinoma (NSCLC) patients. Overexpressed XIAP could degrade through ubiquitination, the mature Smac (show DIABLO ELISA Kits) inhibiting NSCLC apoptosis.
These results indicate that XIAP plays an important physiologic role in regulating sublethal CASP-3 (show CASP3 ELISA Kits) activity within central neurons and thereby facilitates synaptic plasticity and memory acquisition.
XIAP antagonizes the switch from TNFalpha (show TNF ELISA Kits)-induced apoptosis to necroptosis in mouse neutrophils.
Results show that XIAP binds to the C terminus of Ptch1 (show PTCH1 ELISA Kits) and mediates the death-dependent function of Ptch1 (show PTCH1 ELISA Kits).
XIAP modulates ubiquitylation of RIP1 (show RALBP1 ELISA Kits) and suppresses RIP3 (show MPRIP ELISA Kits)-dependent cell death and inflammasome activation in response to TNF (show TNF ELISA Kits)-signaling in innate immune cells.
XIAP deficiency selectively impaired B-cell chronic lymphocytic leukemia/lymphoma 10 (BCL10 (show BCL10 ELISA Kits))-mediated innate responses to dectin-1 (show CLEC7A ELISA Kits) ligands but did not affect responses to various Toll (show TLR4 ELISA Kits)-like receptor agonists.
XIAP mRNA level was also reduced in the BRE (show BRE ELISA Kits)-depleted cells, but the level of reduction was less profound than that of the protein level. However, BRE (show BRE ELISA Kits) could not delay protein turnover of XIAP.
Identify xIAP and cIAP1 (show BIRC2 ELISA Kits) as molecular targets of ceramide and show ceramide analog LCL85 is an effective sensitizer in overcoming resistance of metastatic colon and breast cancers to apoptosis induction to suppress metastasis in vivo.
XIAP-/- DRG sensory neurons degenerate more rapidly and contain more active caspase-3 (show CASP3 ELISA Kits).
XIAP ubiquitylates RIPK2 (show RIPK2 ELISA Kits) and recruits the linear ubiquitin chain assembly complex to NOD2 (show NOD2 ELISA Kits)
XIAP is expressed in oligodendrocytes in vivo and in vitro. Increased XIAP expression is associated with protection against selected cell death pathways, whereas decreased expression increases oligodendroglial cell death.
This gene encodes a protein that belongs to a family of apoptotic suppressor proteins. Members of this family share a conserved motif termed, baculovirus IAP repeat, which is necessary for their anti-apoptotic function. This protein functions through binding to tumor necrosis factor receptor-associated factors TRAF1 and TRAF2 and inhibits apoptosis induced by menadione, a potent inducer of free radicals, and interleukin 1-beta converting enzyme. This protein also inhibits at least two members of the caspase family of cell-death proteases, caspase-3 and caspase-7. Mutations in this gene are the cause of X-linked lymphoproliferative syndrome. Alternate splicing results in multiple transcript variants. Pseudogenes of this gene are found on chromosomes 2 and 11.
X-linked inhibitor of apoptosis protein
, baculoviral IAP repeat-containing 4
, baculoviral IAP-repeat containing protein 4
, Baculoviral IAP repeat-containing protein 4
, E3 ubiquitin-protein ligase XIAP
, X-linked IAP
, IAP-like protein
, baculoviral IAP repeat-containing protein 4
, inhibitor of apoptosis protein 3
, IAP homolog A
, apoptosis inhibitor 3
, apoptosis inhibitor protein 3