Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human KLF9 Antibodies:
anti-Mouse (Murine) KLF9 Antibodies:
anti-Rat (Rattus) KLF9 Antibodies:
Go to our pre-filtered search.
Cow (Bovine) Polyclonal KLF9 Primary Antibody for IHC, WB - ABIN2777263
Imataka, Nakayama, Yasumoto, Mizuno, Fujii-Kuriyama, Hayami: Cell-specific translational control of transcription factor BTEB expression. The role of an upstream AUG in the 5'-untranslated region. in The Journal of biological chemistry 1994
results demonstrated the molecular interaction between miR-378 and KLF9, indicating the therapeutic potential of miR-378 for osteosarcoma.
KLF9 suppressed tumorigenicity of the pancreatic ductal adenocarcinoma by negatively regulating frizzled-5.
KLF9 could down-regulate MMP9 expression to inhibit breast cancer metastasis.
KLF9 status was associated with differentiation and vascular invasion expression and was found to be a valuable prognostic factor for patients with pancreatic ductal adenocarcinoma
In conclusion, LPA plays dual roles as a ligand mediator through the activation of cell surface G-coupled protein receptors and as an intracellular second messenger through the activation of PPARgamma. We discuss the contribution of the LPA1-PPARgamma-KLF9 axis to neurite outgrowth and proliferation in human iPSC-derived neurons.
miR-141-3p/KLF9 may play an important role in regulating the growth of prostate cancer
The expression of KLF9 is down-regulated in esophageal squamous cell carcinoma and inversely correlated with the clinical features.
Suggest role for miR-570/KLF9 molecular network in controlling lung carcinoma progression.
TRs cooperate with KLF9 to regulate hepatocyte proliferation and differentiation and early stages of organogenesis and that TRs exert widespread and important influences on ESC biology.
Myometrial KLF9 may contribute to the onset of human parturition through its regulation of PGR expression and inflammatory signaling networks.
the expression of KLF9 is up-regulated in human ovarian cancer; KLF9 knockdown significantly inhibited cell proliferation and resulted in cell cycle arrest in the G0/G1 phase
In this review, we focus on the functions, roles, and regulatory networks of these five KLFs in HCC, summarize key pathways, and propose areas for further investigation
Palmitic acid increases Ppargamma and Klf6 & Klf9 gene expression and promotes triglyceride accumulation in HepG2 cells.
Reduced KLF9 expression is associated with glioma.
Data indicate that integrin alpha6 repression by Kruppel-like factor-9 (KLF9) inhibits glioblastoma cell stemness and tumorigenicity.
increased KLF9 expression is in part responsible for CYP2D6 induction during pregnancy via the potentiation of HNF4alpha transactivation of CYP2D6.
KLF9 suppresses the growth of hepatocellular carcinoma cells in vivo and positively regulates p53 expression by increasing protein stability.
We confirmed that PDCD5 overexpression stimulated the promoter activities of KLF9 by luciferase reporter assays.
Data collectively show that KLF9 substantially inhibits AKT activation and abrogates tumor growth of PCa cells.
Nrf2 amplifies oxidative stress via induction of Klf9.
Study identified genomic targets of Klf9 in hippocampal neurons which raise some indication about it functions in chromatin, and neuronal morphology regulation and survival across the lifespan.
Kruppel-like factor 9 (KLF9) is a haploinsufficient tumor suppressor in the ApcMin/+ mouse colon by suppressing expression of ISG15, an apoptosis-inhibiting cytokine.
in endometrial stromal cells, KLF9 provides coincident regulation of Notch, Hh, and steroid receptor signaling pathways, which when deregulated, underlie establishment and/or progression of endometriosis
KLF9 bound the KLF binding element at position -874 of the mouse C/EBPbeta promoter.
Klf9 is essential for turning off programmed cell death of Purkinje cells in organotypic cultures.
We showed that Kruppel-like factor 9 was a key mediator of this effect of T(3); the sudden physiological increase in T(3) during development is involved in the onset of the loss of axon regenerative capacity in purkinje cells.
KLF9 is an integral component of the T3-driven signaling cascade that promotes myelin regeneration.
Common variants at CDKAL1 and KLF9 are associated with body mass index in east Asian populations.
KLF9 could synergistically activate PPARgamma2 promoter by directly interacting with C/EBPalpha.
Data support cross-regulation among BMP2, KLF9, and KLF13 to maintain progesterone sensitivity in stromal cells undergoing differentiation and suggest that loss of this network compromises establishment of uterine receptivity and implantation success.
Loss of KLF9 expression resulted in increased glandular ESR1 expression.
These results identify Bteb1 as a functionally relevant progesterone receptor (PR)-interacting protein and suggest its selective modulation of cellular processes that are regulated by PR-A in the uterine stroma.
BTEB1, by regulating ST PGR expression and transactivation, participates in the paracrine control of LE proliferation by PGR and thus is important for establishment of a receptive uterus critical for successful implantation.
Klf9 controls the elaboration, from intestine smooth muscle, of molecular mediator(s) of crypt cell proliferation and lineage determination and of villus cell migration.
Klf9 knockout (KO) mice exhibited delayed parturition by 1-2 days relative to wild-type (WT) counterparts, in the absence of fetal genotype contribution and differences in serum estrogen and progesterone levels.
HNF4alpha regulates thyroid hormone homeostasis through transcriptional regulation of the Dio1 gene with GATA4 and KLF9
Deletion of Klf9 up-regulated uterine Phb2 expression and increased PHB2 nuclear localization in epithelial cells.
The study identifies a functional DR-4 T(3)response element located in the mouse Klf9 gene to explain its regulation by T(3) during mammalian brain development.
Data show that forced expression of Kruppel-like factor 9 (Klf9) in the brain of thyroid-intact tadpoles increased baseline thyroid hormone receptor-beta (trb) mRNA and enhanced trb autoinduction.
Induced expression of BTEB1 in XTC-2 cells caused accelerated and enhanced autoinduction of the TrbetaA gene.
KLF9 was verified to be directly regulated by TH in a TH receptor (TR)-dependent manner in hypothyroid mutants
knockdown of klf9 in zebrafish embryos impaired hematopoietic development including erythroid maturation and T lymphopoiesis
The protein encoded by this gene is a transcription factor that binds to GC box elements located in the promoter. Binding of the encoded protein to a single GC box inhibits mRNA expression while binding to tandemly repeated GC box elements activates transcription.
BTE-binding protein 1
, GC-box-binding protein 1
, Krueppel-like factor 9
, basic transcription element binding protein 1
, basic transcription element-binding protein 1
, transcription factor BTEB1
, Kruppel-like factor 9
, gene 1
, gene 3
, basic transcription element binding protein 1 (gene 1)