Kruppel-Like Factor 5 (Intestinal) (KLF5) ELISA Kits

KLF5 encodes a member of the Kruppel-like factor subfamily of zinc finger proteins. Zusätzlich bieten wir Ihnen KLF5 Antikörper (96) und KLF5 Proteine (6) und viele weitere Produktgruppen zu diesem Protein an.

list all ELISA KIts Gen GeneID UniProt
Anti-Ratte KLF5 KLF5 84410  
KLF5 12224 Q9Z0Z7
KLF5 688 Q13887
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Top KLF5 ELISA Kits auf antikoerper-online.de

Showing 2 out of 5 products:

Katalog Nr. Reaktivität Sensitivität Bereich Bilder Menge Lieferzeit Preis Details
Human 0.059 ng/mL 0.15 ng/mL - 10 ng/mL 96 Tests 13 bis 16 Tage
$700.00
Details
Maus
  96 Tests 15 bis 18 Tage
$875.60
Details

Weitere ELISA Kits für KLF5 Interaktionspartner

Mouse (Murine) Kruppel-Like Factor 5 (Intestinal) (KLF5) Interaktionspartner

  1. Klf5 is essential for mammary gland development and breast tumorigenesis via transcription of Slug.

  2. the available data suggest that the augmentation of endothelial KLF5 expression by hyperinsulinemia may represent a novel mechanism for negatively regulating eNOS expression, and may thus help to explain for the T2DM-related endothelial dysfunction at the transcriptional level

  3. RNAi-mediated depletion of Sp4 and Klf5 decreased Tas1r1 expression, while overexpression of Klf5, but not Sp4, significantly increased Tas1r1 expression in the myoblast cells.

  4. these results show for the first time that Klf5 has a unique role suppressing ERK activity in Mouse embryonic stem cells.

  5. KLF5 expression is elevated in the aortic tissue of atherosclerosis mice, as compared to control mice.

  6. High KLF5 expression may play a pivotal role in the pathogenesis of congenital cystic adenomatoid malformation of the lungs partly through regulating the activity of MMP-9.

  7. These results indicate that Klf5 plays a critical role in the ductular reaction and biliary epithelial tissue expansion and remodeling by inducing biliary epithelial cell proliferation and thereby contributing to liver regeneration.

  8. any one of Klf2, Klf4 and Klf5 was sufficient to support self-renewal of mouse embryonic stem cells, whereas the removal of all three compromised it.

  9. the regulatory crosstalk between KLF5, miR-29a, and Fbw7/CDC4 cooperatively promotes atherosclerotic development

  10. KLF5 as an essential factor required for acinar-to-ductal metaplasia and oncogenic KRAS-induced pancreatic tumor formation.

  11. lf5 ChIP-seq revealed that Klf5 binding overlaps that of MyoD and Mef2, and Klf5 physically associates with both MyoD and Mef2. In addition, MyoD recruitment was greatly reduced in the absence of Klf5. These results indicate that Klf5 is an essential regulator of skeletal muscle differentiation, acting in concert with myogenic transcription factors such as MyoD and Mef2.

  12. KLF5 regulates intestinal barrier function by mediating the transcription of DSG2, a gene encoding a major component of desmosome structures

  13. Klf5 suppresses Fgf4-Fgfr-ERK signalling, thus preventing precocious activation of the primitive endoderm specification programme

  14. In conclusion, the results of this study suggest that the presence of KLF5 in postn-positive cells contributes to the pathogenesis of aortic thickening induced by DOCA-salt hypertension.

  15. these studies demonstrate dual functions of Klf5 in regulating hematopoietic stem and progenitor proliferation and localization in the bone marrow, as well as lineage choice after GMP, promoting increased neutrophil output at the expense of eosinophil production.

  16. Collectively, we identify a novel regulatory pathway in which 1, 25(OH)2D3 induces VDR expression and promotes VDR interaction with p50 subunit of NF-kappaB, which in turn attenuates the association of KLF5 with p50 subunit of NF-kappaB and thus exerts anti-inflammatory and anti-proliferative effects on macrophages.

  17. KLF5-dependent regulation of Myo9b/RhoA is required for podosome formation and macrophage migration during abdominal aortic aneurysm.

  18. Data show that R-Smad Proteins SMAD1 and SMAD5, which transduce bone morphogenetic protein (BMP) signals, recognize enhancer regions together with Kruppel-like factors KLF4 and KLF5 in naive embryonic stem cell (mESCs).

  19. illustrates that KLF5 may modulate DNA repair pathways to prevent intestinal injury induced by TBI. KLF5 signaling provides a novel field for identification of potential therapeutic targets for the treatment of radiation-induced intestinal damage

  20. Cardiac myocyte KLF5 is a transcriptional regulator of Ppara and cardiac energetics.

Human Kruppel-Like Factor 5 (Intestinal) (KLF5) Interaktionspartner

  1. The positive expression rate of LPA2 and KLF5 were statistical different in gastric adenocarcinoma, GIN, and normal gastric tissue (P<0.05). LPA2 positive expression was associated with tumor invasion depth, Lauren type, vascular invasion, local lymph node metastasis, and clinical stage (P<0.05).

  2. Klf5 is essential for mammary gland development and breast tumorigenesis via transcription of Slug.

  3. KLF5 and TNFRSF11a promote cervical cancer cell proliferation, migration and invasiveness.

  4. KLF5 knockdown could suppress hypoxia-induced cisplatin resistance, and its mechanism may be due to the inhibition of HIF-1alpha-dependent glycolysis via inactivation of the PI3K/Akt/mTOR pathway.

  5. The results indicate that KLF5 plays a significant role in hepatocellular carcinoma (HCC) progression and metastasis and induces EMT via activating PI3K/AKT/Snail signaling, and the inhibition of KLF5 may be a potential treatment modality for patients with HCC.

  6. the positive feedback loop of KLF5/CASC15/miR-153-3p/KLF5 in the acceleration of breast cancer malignant behaviors and tumorigenesis, is reported.

  7. these data suggested that the elevated cav-1 promoted pituitary adenoma cells migration and invasion by regulating the interaction between EGR1 and KLF5.

  8. Silencing CINP had the most potent inhibitory effect on cell growth in KLF5-expressing cells but did not affect parental TSU-Pr1 cells. Further analyses not only confirmed the physical interaction between KLF5 and CINP, also demonstrated that knockdown of CINP attenuated the effects of KLF5 on cell cycle progression, apoptosis and tumorigenesis.

  9. The miR-152/KLF5 axis may provide novel therapeutic targets for CC treatment.

  10. PVT1, KLF5, and beta-catenin were also revealed to be co-expressed in clinical TNBC samples.

  11. Was greatly suppressed by the silence of KLF5, GCN5, or GDF15.

  12. KLF5 may play an important role in odontoblast differentiation and dentin formation.

  13. Utilizing data from CRISPR/Cas9 gene knockout screening, authors reveal that cancer cells with KLF5 overexpression are dependent on KLF5 for their proliferation, suggesting KLF5 as a putative therapeutic target.

  14. KLF5 and TNFRSF11a are related to cervical cancer. KLF5 promotes the proliferation, migration, and invasion of cervical cancer cells partly by upregulating the transcription of TNFRSF11a.

  15. These results revealed that KLF5 promotes the tumorigenesis and metastasis of thyroid cancer cells and may be a potential therapeutic target in patients with thyroid cancer

  16. the present findings were the first to show that KLF5 expression and nitration by iNOS-mediated peroxynitrite are necessary for the induction of TNF-alpha and IL-1beta expression in VSMCs of diabetic vascular tissues.

  17. the results of the present study suggested that the miR5905p/KLF5 axis may regulate osteosarcoma (OS)progression and thus, may be a novel therapeutic target for the treatment of patients with OS.

  18. Study showed that KLF5 expression was increased in intracranial aneurysms (IAs) patients compared to that of normal subjects, and KLF5 overexpression vascular smooth muscle cells proliferation, migration, and phenotypic modulation, suggesting that the upregulated KLF5 expression played an important role in the induction of IAs.

  19. correlation between the KLF5 and ZEB1 transcription levels in the pancreatic tumor tissues

  20. The present study has identified that KLF5, a target of miR-145-5p, is a key marker gene in cancer. miR-145-5p may also contribute to the dysregulation of other functional genes during tumor development.

KLF5 Antigen-Profil

Beschreibung des Gens

This gene encodes a member of the Kruppel-like factor subfamily of zinc finger proteins. Since the protein localizes to the nucleus and binds the epidermal growth factor response element, it is thought to be a transcription factor.

Genbezeichner und Symbole assoziert mit KLF5

  • Kruppel like factor 5 (KLF5) Antikörper
  • Kruppel-like factor 5 (intestinal) S homeolog (klf5.S) Antikörper
  • Kruppel-like factor 5 (Klf5) Antikörper
  • 4930520J07Rik Antikörper
  • bteb2 Antikörper
  • CKLF Antikörper
  • IKLF Antikörper
  • klf5 Antikörper
  • MGC115081 Antikörper

Bezeichner auf Proteinebene für KLF5

Kruppel-like factor 5 (intestinal) , Krueppel-like factor 5-like , Kruppel-like factor 5 , basic-transcription-element-binding-protein 2 , basic transcription element binding protein 2 , basic transcription element binding protein BTEB2 , BTE-binding protein 2 , Krueppel-like factor 5 , basic transcription element-binding protein 2 , intestinal-enriched krueppel-like factor , transcription factor BTEB2 , GC box binding protein 2 , GC-box-binding protein 2 , colon krueppel-like factor , colon kruppel-like factor , intestinal-enriched kruppel-like factor

GENE ID SPEZIES
100052058 Equus caballus
452597 Pan troglodytes
100010455 Monodelphis domestica
100231095 Taeniopygia guttata
100467044 Ailuropoda melanoleuca
100607414 Nomascus leucogenys
735138 Xenopus laevis
100008718 Oryctolagus cuniculus
84410 Rattus norvegicus
12224 Mus musculus
688 Homo sapiens
418818 Gallus gallus
612788 Canis lupus familiaris
100038005 Sus scrofa
535702 Bos taurus
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