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During prostate cancer initiation, Nkx3.1 expression is frequently lost in both humans and mouse models. Data, including data from studies using cells from transgenic mice, suggest that androgens activate Nkx3.1 transcription via androgen receptor (zeige AR ELISA Kits) binding to 11-kb region in both normal luminal cells and castration-resistant prostatic neoplasm cells via androgen response elements in Nkx3.1 3prime untranslated region.
study demonstrated that expression of homeobox protein NK-3 homolog A(Nkx3.1) influenced both the timing and magnitude of the DNA damage response in the mouse prostate
Nkx3.1 loss and Tmprss2 (zeige TMPRSS2 ELISA Kits)-ERG (zeige ERG ELISA Kits) upregulation do not cooperate to enhance prostate tumorigenesis in vivo.
Id4 regulates NKX3.1, Sox9 and PTEN.
activated canonical Wnt (zeige WNT2 ELISA Kits) signals and Nkx3.1 function in a positive feedback loop to regulate prostate bud growth and luminal epithelial differentiation.
multiple NKX3.1 binding sites were found in the RAMP1 (zeige RAMP1 ELISA Kits) locus in human prostate cancer cells and in the normal mouse prostate.
Deletions of Klf5 (zeige KLF5 ELISA Kits) and Nkx3-1 do not have a additive effect in prostatic carcinogenesis in mouse model.
Transcriptional activation of prostate specific homeobox (zeige PRRX1 ELISA Kits) gene NKX3-1 in subsets of T-cell lymphoblastic leukemia (T-ALL).
Androgen-dependent transcription of the mouse Nkx3.1 gene is conferred through a noncanonical element within the intron of the gene.
Nkx3.1 has a role in bacterial prostatitis and its progression to inflammation and neoplasia
With deletion mutation analysis, plasmid construction, EMSA and oligonucleotide decoy technique, two Sp1 (zeige PSG1 ELISA Kits)-elements which located between +29 to +43 and -60 to -46 of NKX3.1 gene were identified and proven to be functional elements.
The androgen-regulated homeodomain transcription factor NKX3.1 plays roles in early prostate development and functions as a prostate-specific tumor suppressor.
the association between the down-regulation of PTEN and NKX3.1 genes contributed to prostate tumorigenesis.
NKX3.1 and DYRK1B (zeige DYRK1B ELISA Kits) were shown to interact via the DYRK1B (zeige DYRK1B ELISA Kits) kinase domain. In vitro kinase assay showed that DYRK1B (zeige DYRK1B ELISA Kits) phosphorylated NKX3.1 at serine 185, a residue critical for NKX3.1 steady-state turnover.
An NKX3.1 binding site polymorphism in the l-plastin (zeige LCP1 ELISA Kits) promoter leads to differential gene expression in human prostate cancer
Analysis of prostate cancer tissues showed that the presence of a TMPRSS2 (zeige TMPRSS2 ELISA Kits)-ERG (zeige ERG ELISA Kits) rearrangement was highly correlated with lower levels of NKX3.1 expression consistent with the role of NKX3.1 as a suppressor of the pathogenic gene rearrangement.
NKX3.1 expression mediate beta-catenin (zeige CTNNB1 ELISA Kits) and E-cadherin (zeige CDH1 ELISA Kits) association and cell migration in prostate cells.
Our results indicate that variation in NKX3.1 expression combined with selenium or vitamin E treatment modifies the risk of prostate cancer.
This gene encodes a homeobox-containing transcription factor. This transcription factor functions as a negative regulator of epithelial cell growth in prostate tissue. Aberrant expression of this gene is associated with prostate tumor progression. Alternate splicing results in multiple transcript variants of this gene.
NK3 transcription factor related, locus 1
, NK3 homeobox 1
, Drosophila NK-3 transcription factor, locus 1
, homeobox protein NK-3 homolog A
, homeobox protein Nkx-3.1
, NK homeobox, family 3, A
, NK3 transcription factor homolog A
, NK-3 transcription factor, locus 1