DYRK1B Antibody
-
货号:CSB-PA908230
-
规格:¥2024
-
图片:
-
其他:
产品详情
-
产品名称:Rabbit anti-Homo sapiens (Human) DYRK1B Polyclonal antibody
-
Uniprot No.:Q9Y463
-
基因名:DYRK1B
-
宿主:Rabbit
-
反应种属:Human,Mouse
-
免疫原:Synthesized peptide derived from internal of Human DYR1B.
-
免疫原种属:Homo sapiens (Human)
-
克隆类型:Polyclonal
-
纯化方式:The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
-
浓度:It differs from different batches. Please contact us to confirm it.
-
产品提供形式:Liquid
-
应用范围:ELISA,WB
-
推荐稀释比:
Application Recommended Dilution WB 1:500-1:3000 -
Protocols:
-
储存条件:Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
-
货期:Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
相关产品
靶点详情
-
功能:Dual-specificity kinase which possesses both serine/threonine and tyrosine kinase activities. Enhances the transcriptional activity of TCF1/HNF1A and FOXO1. Inhibits epithelial cell migration. Mediates colon carcinoma cell survival in mitogen-poor environments. Inhibits the SHH and WNT1 pathways, thereby enhancing adipogenesis. In addition, promotes expression of the gluconeogenic enzyme glucose-6-phosphatase catalytic subunit 1 (G6PC1).
-
基因功能参考文献:
- Dyrk1B was overexpressed in breast cancer tissues and cells and correlates with FoxO1 phosphorylation and cell proliferation. PMID: 28554575
- High DYRK1B expression is associated with pancreatic and skin cancers. PMID: 26784250
- The study shows that DYRK1B is a novel ERK2 substrate, uncovering new links between two kinases involved in cell fate decisions. PMID: 26346493
- Data reveal a novel role for miR-9 in regulation of the NFAT pathway by targeting KPNB1 and DYRK1B. PMID: 25696812
- NKX3.1 and DYRK1B were shown to interact via the DYRK1B kinase domain. In vitro kinase assay showed that DYRK1B phosphorylated NKX3.1 at serine 185, a residue critical for NKX3.1 steady-state turnover. PMID: 25777618
- Upregulation of Mirk mRNA expression is mediated by CREB binding to two sites in the Mirk promoter upstream of the transcription start site and one site within exon 4. PMID: 24590896
- A founder mutation was identified in DYRK1B, substituting cysteine for arginine at position 102 in 3 families with metabolic syndrome. PMID: 24827035
- DYRK1B is a novel Thr(286)-CCND1 kinase that acts independently of GSK3beta to promote CCND1 degradation. PMID: 24134204
- Mirk/Dyrk1B plays an important role in ovarian cancer cell survival through modulating FoxO translocation. PMID: 22159921
- In line with a redirection of autocrine toward paracrine HH signaling by a KRAS-DYRK1B network, we find high levels of GLI1 expression restricted to the stromal compartment and not to SHH-expressing tumor cells in pancreatic adenocarcinoma. PMID: 20512148
- the kinase Mirk is essential for the growth and survival of osteosarcoma cells. PMID: 20042639
- activation by MKK2 and role as transcriptional activator of HNF1alpha PMID: 11980910
- p38 MAP Kinase suppresses the function of Mirk as a transcriptional activator only when cells are proliferating PMID: 12384504
- Mirk is anti-apoptotic in myoblasts PMID: 15851482
- Mirk is a survival factor for pancreatic ductal adenocarcinoma. Because knockout of Mirk does not cause embryonic lethality, Mirk is not essential for normal cell growth. PMID: 16618736
- This review summarizes the known regulators and functions of Mirk kinase and outlines opportunities for future studies of Mirk in the fields of muscle and tumor biology. PMID: 16845176
- GSK-3beta but also DYRK1B modulates cyclin D1 subcellular localization by the phosphorylation of Thr(288). These results suggest that DIF-3 induces degradation of cyclin D1 through the GSK-3beta- and DYRK1B-mediated threonine phosphorylation in HeLa cells PMID: 17046823
- BCL2 and BCL-xL facilitation of G0 quiescence requires BAX, BAK, and p27 phosphorylation by Mirk PMID: 18818203
- Quiescent pancreatic cancer cells depleted of Mirk became less viable because they were damaged by ROS, and had increased levels of G(1) cyclins to prime cells to escape quiescence. PMID: 19351855
- Mirk, through regulating cyclin D turnover, and the CDK inhibitor p27, as shown by depletion studies, functioned independently and additively to regulate the exit of tumor cells from quiescence. PMID: 19542220
显示更多
收起更多
-
相关疾病:Abdominal obesity-metabolic syndrome 3 (AOMS3)
-
亚细胞定位:Nucleus.
-
蛋白家族:Protein kinase superfamily, CMGC Ser/Thr protein kinase family, MNB/DYRK subfamily
-
组织特异性:Highest expression in skeletal muscle, testis, heart and brain with little expression in colon or lung. Expressed in a variety of tumor cell lines.
-
数据库链接:
HGNC: 3092
OMIM: 604556
KEGG: hsa:9149
STRING: 9606.ENSP00000312789
UniGene: Hs.130988
Most popular with customers
-
-
YWHAB Recombinant Monoclonal Antibody
Applications: ELISA, WB, IF, FC
Species Reactivity: Human, Mouse, Rat
-
Phospho-YAP1 (S127) Recombinant Monoclonal Antibody
Applications: ELISA, WB, IHC
Species Reactivity: Human
-
-
-
-
-