STK36 & GLI3 Protein Protein Interaction Antibody Pair
- Known as:
- STK36 & GLI3 Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0590
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- STK36 & GLI3 Protein Interaction Antibody Pair
Ask about this productRelated genes to: STK36 & GLI3 Protein Protein Interaction Antibody Pair
- Gene:
- GLI3 NIH gene
- Name:
- GLI family zinc finger 3
- Previous symbol:
- GCPS, PHS
- Synonyms:
- PAP-A, PAPA, PAPA1, PAPB, ACLS, PPDIV
- Chromosome:
- 7p14.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-29
- Date modifiied:
- 2016-10-05
- Gene:
- STK36 NIH gene
- Name:
- serine/threonine kinase 36
- Previous symbol:
- -
- Synonyms:
- KIAA1278, FU
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-22
- Date modifiied:
- 2015-08-26
Related products to: STK36 & GLI3 Protein Protein Interaction Antibody Pair
Related articles to: STK36 & GLI3 Protein Protein Interaction Antibody Pair
- Hedgehog (Hh) signaling culminates in the conversion of the latent transcription factor Cubitus interruptus (Ci)/Gli from a repressor form (Ci/Gli) into an activator form (Ci/Gli). While sequential phosphorylation of Ci/Gli by protein kinase A(PKA), glycogen synthase kinase 3 (GSK3), and casein kinase 1 (CK1) is essential for its proteolytic processing that generates Ci/Gli, sequential phosphorylation of Ci/Gli by the Fused (Fu)/Unc-51 like kinase (Ulk) family kinases Fu/Ulk3/Stk36 and CK1 contributes to the formation of Ci/Gli. Fu/Ulk3/Stk36-mediated phosphorylation of Ci/Gli is stimulated by Hh, leading to altered interaction between Ci/Gli and the Hh pathway repressor Sufu. Here we describe both in vitro and in vivo assays that determine Ci/Gli phosphorylation by the Fu/Ulk family kinases and its regulation by Hh. - Source: PubMed
Han YuhongJiang Jin - Hypospadias is one of the most common congenital anomalies of the male genitalia. Sonic hedgehog homologue (SHH) signalling pathway is believed to be involved in the development of the male genital system. - Source: PubMed
Publication date: 2021/06/30
Saraç MehmetCanpolat ŞenayÖnalan Etem EbruTektemur AhmetTartar TugayBakal UnalKazez Ahmet - SHH (Sonic Hedgehog)-GLI signaling plays an important role during embryogenesis and in tumorigenesis. The survival and growth of several types of cancer depend on autonomously activated SHH-GLI signaling. A protein complex containing the ubiquitin ligase MID1 and protein phosphatase 2A regulates the nuclear localization and transcriptional activity of GLI3, a transcriptional effector molecule of SHH, in cancer cell lines with autonomously activated SHH signaling. However, the exact molecular mechanisms that mediate the interaction between MID1 and GLI3 remained unknown. Here, we show that MID1 catalyzes the ubiquitination and proteasomal cleavage of the GLI3 regulator Fu. Our data suggest that Fu ubiquitination and cleavage is one of the key elements connecting the MID1-PP2A protein complex with GLI3 activity control. - Source: PubMed
Publication date: 2014/10/02
Schweiger SusannDorn StephanieFuchs MelanieKöhler AndreaMatthes FrankMüller Eva-ChristinaWanker ErichSchneider RainerKrauß Sybille - Hedgehog, WNT, FGF and BMP signaling pathways network together during embryogenesis, tissue regeneration, and carcinogenesis. Aberrant activation of Hedgehog signaling pathway leads to pathological consequences in a variety of human tumors, such as gastric cancer and pancreatic cancer. Endoscopic mucosal resection (EMR), endoscopic submucosal dissection (ESD), surgical gastrectomy and chemotherapy are therapeutic options for gastric cancer; however, prognosis of advanced gastric cancer patient is still poor. Here, Hedgehog signaling pathway in human gastric cancer and its clinical applications will be reviewed. Human SHH, IHH, DHH (Hedgehog homologs), HHAT (Hedgehog acyltransferase), HHIP (Hedgehog-interacting protein), DISP1, DISP2, DISP3 (Dispatched homologs), PTCH1, PTCH2 (Patched homologs), SMO (Smoothened homolog), KIF27, KIF7 (Costal-2 homologs), STK36 (Fused homolog), SUFU (SuFu homolog), DZIP1 (Iguana homolog), GLI1, GLI2 and GLI3 (Cubitus interruptus homologs) are implicated in the Hedgehog signaling. PTCH1, FOXM1 and CCND2 are direct transcriptional targets of Hedgehog signaling. Hedgehog signaling activation leads to cell proliferation through cell cycle regulation. SHH regulates growth and differentiation within gastric mucosa through autocrine loop and FOXL1-mediated epithelial-mesenchymal interaction. SHH is implicated in stem/progenitor cell restitution of damaged gastric mucosa during chronic infection with Helicobacter pylori. SHH up-regulation, IHH upregulation and HHIP down-regulation lead to aberrant activation of Hedgehog signaling through PTCH1 to GLI1 in gastric cancer. Small molecule compounds targeted to SMO (KADD-cyclopamine, SANT1-4, Cur61414) as well as humanized anti-SHH antibodies are potent anti-cancer drugs for gastric cancer. Cocktail of Hedgehog inhibitors would be developed as novel therapeutics for gastric cancer. Single nucleotide polymorphism (SNP) and copy number polymorphism (CNP) of Hedgehog signaling genes would be utilized for genetic screening of gastric cancer, while cDNA-PCR, microarray and ELISA detecting aberrant Hedgehog signaling activation would be utilized for therapeutic optional choice. Genetic screening and precise selection of therapeutic options would contribute to the realization of personalized medicine. - Source: PubMed
Publication date: 2005/10/18
Katoh YurikoKatoh Masaru