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SLC7A11 encodes a member of a heteromeric, sodium-independent, anionic amino acid transport system that is highly specific for cysteine and glutamate. Zusätzlich bieten wir Ihnen SLC7A11 Antikörper (101) und SLC7A11 Kits (18) und viele weitere Produktgruppen zu diesem Protein an.
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the level of antisense SLC7A11 was markedly reduced in epithelial ovarian cancer tissues and cell lines compared with those of normal control; reduction of antisense SLC7A11 level prompted ovarian cancer cell migration mainly by suppressing the expression of SLC7A11
CD44v9 in tumor specimens has potential as a novel indicator for identifying a cisplatin-chemoresistant population among urothelial cancer patients. CD44v8-10 contributes to reactive oxygen species defenses, which are involved in chemoresistance, by promoting the function of xCT, which adjusts the synthesis of glutathione.
Oncogenic PIK3CA (zeige PIK3CA Proteine) alters methionine and cysteine utilization, partly by inhibiting xCT to contribute to the methionine dependency phenotype in human breast cancer cells.
these observations suggest that SLC7A11 may be a vital biomarker for the diagnosis and prognosis in human laryngeal squamous cell carcinoma (LSCC) and targeting SLC7A11 appears to be a potentially significant method for LSCC treatment.
Aberrant neuronal or neuroendocrine system may be involved in the suppressed reproductive performance in xCT deficient male mice.
overexpression of SLC7A11 in the context of glioblastoma multiforme may contribute to tumor progression.
miR (zeige MLXIP Proteine)-375 served as a tumor suppressor via regulating SLC7A11.
As targets of oncogenes with intrinsic tyrosine kinase (zeige TXK Proteine) activity, STAT3 (zeige STAT3 Proteine) and STAT5 (zeige STAT5A Proteine) become constitutively active in hematologic neoplasms and solid tumors, promoting cell proliferation and survival and modulating redox homeostasis via regulation xCT expression. (Review)
Authors found that the xCT expression was increased in peripheral blood monocyte of active tuberculosis. xCT expression in macrophage was induced by Mycobacterium tuberculosis (Mtb (zeige NCAPG2 Proteine)) through TLR2/Akt (zeige AKT1 Proteine)- and p38 (zeige CRK Proteine)-dependent signaling pathway.
Genetic and pharmacological inhibition of xCT potentiated the cytotoxic effects of aspirin plus sorafenib; this effect was diminished by xCT overexpression. Low-dose aspirin plus sorafenib enhanced the cytotoxicity of cisplatin in resistant HNC (zeige MMP8 Proteine) cells through xCT inhibition and oxidant and DNA damage.
Protein expression of xCT is enhanced in immune cells from an animal model of multiple sclerosis.
Study suggests that mature astrocytes have low expression levels of xCT and that they do not depend on its function to survive. In contrast, oligodendrocytes, which express high levels of xCT, are the most vulnerable cell type of CNS to glutathione depletion upon chronic blockage of xCT or under oxidative glutamate (zeige GRIN1 Proteine) toxicity.
ARF inhibits tumor growth by suppressing the ability of NRF2 (zeige NFE2L2 Proteine) to transcriptionally activate its target genes, including SLC7A11, a component of the cystine/glutamate (zeige GRIN1 Proteine) antiporter that regulates reactive oxygen species (ROS (zeige ROS1 Proteine))-induced ferroptosis.
Expression of xCT is reduced in astroglia in a genetic mouse model of susceptibility to depressive-like behavior.
Data suggest that glucose starvation of various neoplasm cell lines induces Slc7a11 expression; Slc7a11 overexpression decreases intracellular glutamate (zeige GRIN1 Proteine), an alternative source of metabolic energy; provision of alpha-ketoglutarate, a key downstream metabolite of glutamate (zeige GRIN1 Proteine), restores survival in Slc7a11-overexpressing neoplasm cell lines under glucose starvation.
HIF-1alpha (zeige HIF1A Proteine) plays a role in cerebral ischaemia-reperfusion -induced glutamate (zeige GRIN1 Proteine) excitotoxicity via the long-lasting activation of system xc(-) -dependent glutamate (zeige GRIN1 Proteine) outflow
Results provided important insights into understanding the mechanism associated with xCT deficiency.
Protein expression of xCT was observed throughout the forebrain and amygdala.
Cerebellar astroglia isolated from Atm (zeige ATM Proteine) mutant mice show decreased expression of the cystine/glutamate (zeige GRIN1 Proteine) exchanger subunit xCT, glutathione reductase (zeige GSR Proteine), and glutathione-S-transferase (zeige GSTa2 Proteine)
This gene encodes a member of a heteromeric, sodium-independent, anionic amino acid transport system that is highly specific for cysteine and glutamate. In this system, designated Xc(-), the anionic form of cysteine is transported in exchange for glutamate. This protein has been identified as the predominant mediator of Kaposi sarcoma-associated herpesvirus fusion and entry permissiveness into cells. Also, increased expression of this gene in primary gliomas (compared to normal brain tissue) was associated with increased glutamate secretion via the XCT channels, resulting in neuronal cell death.
solute carrier family 7, (cationic amino acid transporter, y+ system) member 11
, cystine/glutamate transporter
, solute carrier family 7, member 11
, Cystine/glutamate transporter
, cystine/glutamate transporter-like
, solute carrier family 7 (anionic amino acid transporter light chain, xc- system), member 11
, amino acid transport system xc-
, calcium channel blocker resistance protein CCBR1
, solute carrier family 7 member 11
, solute carrier family 7 (cationic amino acid transporter, y+ system), member 11
, cysteine/glutamate transporter
, sodium independent anionic amino acid transport system