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anti-Human XIAP Antibodies:
anti-Mouse (Murine) XIAP Antibodies:
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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 (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 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 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
In a systematic analysis of variants in 23 primary immuno-deficiencies-associated genes, study confirmed the association of variants in XIAP with Crohn's disease.
These results reveal that RPS3 (show RPS3 Antibodies) upregulates XIAP independently of the NF-kappaB (show NFKB1 Antibodies) pathway in human breast cancer cells
downregulation of XIAP expression could enhance the sensitivity of RCC (show XRCC1 Antibodies) cells to apoptosis, and the basal expression of XIAP during apoptosis is stable.
XIAP promotes ubiquitylation and degradation of Bcl-2 (show BCL2 Antibodies).
XIAP gene silencing would strengthen the radiosensitivity of esophageal cancer cells in vivo and in vitro, which provides a novel (show CASP3 Antibodies)target for the (show CASP9 Antibodies) treatment of esophageal cancer.
Findings of the study confirm that L-THP (show UMOD Antibodies) resulted in p53 (show TP53 Antibodies) independent apoptosis via down-regulating XIAP protein by inhibiting MDM2 (show MDM2 Antibodies) associated with proteasome-dependent pathway and increased sensitivity of EU-4 cells against doxorubicin.
miR (show MLXIP Antibodies)-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 (show PIK3CA Antibodies) 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
mRNA and protein expressions of XIAP were decreased via siRNA targetting, which leads to increases in cell apoptosis and caspase-3 (show CASP3 Antibodies) and caspase-9 (show CASP9 Antibodies) 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 (show FAIM Antibodies) protein (FAIM (show FAIM Antibodies)-L) is a death receptor antagonist that stabilizes XIAP protein levels, thus preventing death receptor-induced neuronal apoptosis. Here we show that FAIM (show FAIM Antibodies)-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 (show TNF Antibodies)-TNFR2 (show TNFRSF1B Antibodies) axis drives cIAP1 (show BIRC2 Antibodies)-TRAF2 (show TRAF2 Antibodies) degradation to allow TLR or TNFR1 (show TNFRSF1A Antibodies) activation of RIPK3 (show RIPK3 Antibodies)-caspase-8 (show CASP8 Antibodies) and IL-1beta (show IL1B Antibodies). 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 (show IL17A Antibodies)-producing CD4 (show CD4 Antibodies) 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 (show IL17A Antibodies)-producing cells from either naive CD4 (show CD4 Antibodies) T cells or Treg cells.
Drugs targeting XIAP and cIAP1 (show BIRC2 Antibodies)/2 may be effective for osteosarcoma patients whose tumors express abundant RIPK1 (show RIPK1 Antibodies) and contain high levels of TNFalpha (show TNF Antibodies).
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 (show CASP3 Antibodies) activity within central neurons and thereby facilitates synaptic plasticity and memory acquisition.
XIAP antagonizes the switch from TNFalpha (show TNF Antibodies)-induced apoptosis to necroptosis in mouse neutrophils.
Results show that XIAP binds to the C terminus of Ptch1 (show PTCH1 Antibodies) and mediates the death-dependent function of Ptch1 (show PTCH1 Antibodies).
XIAP modulates ubiquitylation of RIP1 (show RALBP1 Antibodies) and suppresses RIP3 (show MPRIP Antibodies)-dependent cell death and inflammasome activation in response to TNF (show TNF Antibodies)-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