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Human Polyclonal XIAP Primary Antibody for IF (cc), IF (p) - ABIN674364
Chen, Bai, Zhong, Xie, Long, Yang, Wu, Jia, Wang: Wogonin has multiple anti-cancer effects by regulating c-Myc/SKP2/Fbw7? and HDAC1/HDAC2 pathways and inducing apoptosis in human lung adenocarcinoma cell line A549. in PLoS ONE 2013
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Human Polyclonal XIAP Primary Antibody for IHC, ELISA - ABIN1003492
Schimmer: Inhibitor of apoptosis proteins: translating basic knowledge into clinical practice. in Cancer research 2004
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Human Polyclonal XIAP Primary Antibody for IHC, IHC (p) - ABIN4366393
Lee, Jiffar, Kupferman: A novel role for BDNF-TrkB in the regulation of chemotherapy resistance in head and neck squamous cell carcinoma. in PLoS ONE 2012
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Human Polyclonal XIAP Primary Antibody for IHC (p), WB - ABIN3044425
Li, Zhang, Fang, Yan, Zhao, Feng, Ma, Ye: Aspirin overcomes Navitoclax-resistance in hepatocellular carcinoma cells through suppression of Mcl-1. in Biochemical and biophysical research communications 2013
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Human Polyclonal XIAP Primary Antibody for ICC, IF - ABIN4366395
Fann, Lee, Manzanero, Tang, Gelderblom, Chunduri, Bernreuther, Glatzel, Cheng, Thundyil, Widiapradja, Lok, Foo, Wang, Li, Drummond, Basta, Magnus, Jo, Mattson, Sobey, Arumugam: Intravenous immunoglobulin suppresses NLRP1 and NLRP3 inflammasome-mediated neuronal death in ischemic stroke. in Cell death & disease 2013
These results reveal that RPS3 (显示 RPS3 抗体) upregulates XIAP independently of the NF-kappaB (显示 NFKB1 抗体) pathway in human breast cancer cells
downregulation of XIAP expression could enhance the sensitivity of RCC (显示 XRCC1 抗体) cells to apoptosis, and the basal expression of XIAP during apoptosis is stable.
XIAP promotes ubiquitylation and degradation of Bcl-2 (显示 BCL2 抗体).
XIAP gene silencing would strengthen the radiosensitivity of esophageal cancer cells in vivo and in vitro, which provides a novel (显示 CASP3 抗体)target for the (显示 CASP9 抗体) treatment of esophageal cancer.
Findings of the study confirm that L-THP (显示 UMOD 抗体) resulted in p53 (显示 TP53 抗体) independent apoptosis via down-regulating XIAP protein by inhibiting MDM2 (显示 MDM2 抗体) associated with proteasome-dependent pathway and increased sensitivity of EU-4 cells against doxorubicin.
miR (显示 MLXIP 抗体)-23a induces trophoblast cell apoptosis by inhibiting XIAP, which may contribute to Preeclampsia.
These data suggest that XIAP may be playing an important role in the pathogenesis of breast cancer and can be therapeutically targeted either alone or in combination with PI3-kinase (显示 PIK3CA 抗体) inhibition to induce efficient apoptosis in breast cancer cells.
loss of XIAP enhances filopodia formation in a Cdc42-dependent manner and this phenomenon phenocopies EGF stimulation. Further, XIAP depletion promotes lung colonization of tumor cells in mice in a Cdc42-dependent manner. These observations shed molecular insights into ubiquitin-dependent regulation of Cdc42 and that of actin cytoskeleton.
XIAP role in the cisplatin resistance in colon cancer
Here, the authors show that transcriptional regulator interacting with the PHD-bromodomain 1 (TRIP-Br1 (显示 SERTAD1 抗体), Sertad1 (显示 SERTAD1 抗体)), a newly identified protein with poorly characterized functions, acts as an adaptor that bridges the interaction of multiple Adenylyl cyclase isoforms with X-linked inhibitor of apoptosis protein (XIAP), a RING-domain E3 ubiquitin ligase (显示 MUL1 抗体).
mRNA and protein expressions of XIAP were decreased via siRNA targetting, which leads to increases in cell apoptosis and caspase-3 (显示 CASP3 抗体) and caspase-9 (显示 CASP9 抗体) activity. It also contributed to the reduced tumor size and tumor weight in a nude mice model of esophageal cancer.
The neuron-specific form of FAIM (显示 FAIM 抗体) protein (FAIM (显示 FAIM 抗体)-L) is a death receptor antagonist that stabilizes XIAP protein levels, thus preventing death receptor-induced neuronal apoptosis. Here we show that FAIM (显示 FAIM 抗体)-L modulates synaptic transmission, prevents chemical-LTD induction in hippocampal neurons, and thwarts axon degeneration after nerve growth factor (NGF) withdrawal.
These data reveal how, upon XIAP deficiency, a TLR-TNF (显示 TNF 抗体)-TNFR2 (显示 TNFRSF1B 抗体) axis drives cIAP1 (显示 BIRC2 抗体)-TRAF2 (显示 TRAF2 抗体) degradation to allow TLR or TNFR1 (显示 TNFRSF1A 抗体) activation of RIPK3 (显示 RIPK3 抗体)-caspase-8 (显示 CASP8 抗体) and IL-1beta (显示 IL1B 抗体). This mechanism may explain why XIAP-deficient patients can exhibit symptoms reminiscent of patients with activating inflammasome mutations.
There was a significantly decreased percentage of IL-17A (显示 IL17A 抗体)-producing CD4 (显示 CD4 抗体) T cells in mice receiving Tregs from xIAP mice. xIAP appears dispensable for the generation of induced Treg cells as well as function of natural Treg cells. There appeared to be a role of xIAP in generation of IL-17 (显示 IL17A 抗体)-producing cells from either naive CD4 (显示 CD4 抗体) T cells or Treg cells.
Drugs targeting XIAP and cIAP1 (显示 BIRC2 抗体)/2 may be effective for osteosarcoma patients whose tumors express abundant RIPK1 (显示 RIPK1 抗体) and contain high levels of TNFalpha (显示 TNF 抗体).
Deletion of XIAP switches cell death away from necrosis to apoptosis.
These results indicate that XIAP plays an important physiologic role in regulating sublethal CASP-3 (显示 CASP3 抗体) activity within central neurons and thereby facilitates synaptic plasticity and memory acquisition.
XIAP antagonizes the switch from TNFalpha (显示 TNF 抗体)-induced apoptosis to necroptosis in mouse neutrophils.
Results show that XIAP binds to the C terminus of Ptch1 (显示 PTCH1 抗体) and mediates the death-dependent function of Ptch1 (显示 PTCH1 抗体).
XIAP modulates ubiquitylation of RIP1 (显示 RALBP1 抗体) and suppresses RIP3 (显示 MPRIP 抗体)-dependent cell death and inflammasome activation in response to TNF (显示 TNF 抗体)-signaling in innate immune cells.
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.
E3 ubiquitin-protein ligase XIAP
, IAP-like protein
, X-linked IAP
, baculoviral IAP repeat-containing protein 4
, inhibitor of apoptosis protein 3
, Baculoviral IAP repeat-containing protein 4
, X-linked inhibitor of apoptosis protein
, baculoviral IAP repeat-containing 4
, baculoviral IAP-repeat containing protein 4
, IAP homolog A
, apoptosis inhibitor 3
, apoptosis inhibitor protein 3
, baculoviral IAP repeat containing 8