STK36 & GLI1 Protein Protein Interaction Antibody Pair
- Known as:
- STK36 & GLI1 Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0589
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- STK36 & GLI1 Protein Interaction Antibody Pair
Related genes to: STK36 & GLI1 Protein Protein Interaction Antibody Pair
- Gene:
- GLI1 NIH gene
- Name:
- GLI family zinc finger 1
- Previous symbol:
- GLI
- Synonyms:
- -
- Chromosome:
- 12q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-01-15
- 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 & GLI1 Protein Protein Interaction Antibody Pair
Related articles to: STK36 & GLI1 Protein Protein Interaction Antibody Pair
- The Hedgehog (Hh) family of secreted proteins governs embryonic development and adult tissue homeostasis through the Gli family of transcription factors. Gli is thought to be activated at the tip of primary cilium, but the underlying mechanism has remained poorly understood. Here, we show that nc-51-ike inase 4 (Ulk4), a pseudokinase and a member of the Ulk kinase family, acts in conjunction with another Ulk family member Stk36 to promote Gli2 phosphorylation and Hh pathway activation. Ulk4 interacts with Stk36 through its N-terminal region containing the pseudokinase domain and with Gli2 via its regulatory domain to bridge the kinase and substrate. Although dispensable for Hh-induced Stk36 kinase activation, Ulk4 is essential for Stk36 ciliary tip localization, Gli2 phosphorylation, and activation. In response to Hh, both Ulk4 and Stk36 colocalize with Gli2 at ciliary tip, and Ulk4 and Stk36 depend on each other for their ciliary tip accumulation. We further show that ciliary localization of Ulk4 depends on Stk36 kinase activity and phosphorylation of Ulk4 on Thr1023, and that ciliary tip accumulation of Ulk4 is essential for its function in the Hh pathway. Taken together, our results suggest that Ulk4 regulates Hh signaling by promoting Stk36-mediated Gli2 phosphorylation and activation at ciliary tip. - Source: PubMed
Publication date: 2023/12/14
Zhou MengmengHan YuhongJiang Jin - 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 - Sonic Hedgehog (Shh) signaling pathway is implicated in various developmental and postnatal processes. Much of the current knowledge about the mechanisms of Shh signal transduction in vertebrates comes from the investigations of the respective pathway in fruit fly Drosophila melanogaster. In Drosophila, serine/threonine kinase fused is involved in all aspects of regulation of the Hh-dependent transcription factor cubitus interruptus possessing both catalytic and regulatory functions. Two proteins, Stk36 and Ulk3, share similarity with fu and have been suggested as mammalian fu homologues. However, in vivo data clarify that Stk36 is not required for embryonic development in mice and participates in Shh-independent genesis of motile cilia. Even if Stk36 is associated with any pathological or physiological aspect of postnatal Shh signaling in mammals, it has perhaps only regulatory functions since its catalytic activity seems to be lost during evolution. In contrast to Stk36, Ulk3 is an active kinase. In non-stimulated cells, Ulk3 catalytic activity is blocked, and it is involved in negative control of Gli proteins, mediators of Shh signaling. In response to Shh, Ulk3 positively regulates Gli proteins by directly phosphorylating them. Thus, Ulk3 is able to recapitulate both positive and negative roles of fu in vitro. However, Ulk3 functioning in vivo remains to be investigated. - Source: PubMed
Maloverjan AllaPiirsoo Marko - Hedgehog, BMP/TGFbeta, FGF, WNT and Notch signaling pathways constitute the stem cell signaling network, which plays a key role in a variety of processes, such as embryogenesis, maintenance of adult tissue homeostasis, tissue repair during chronic persistent inflammation, and carcinogenesis. Sonic hedgehog (SHH), Indian hedgehog (IHH) and Desert hedgehog (DHH) bind to PTCH1/PTCH or PTCH2 receptor to release Smoothened (SMO) signal transducer from Patched-dependent suppression. SMO then activates STK36 serine/threonine kinase to stabilize GLI family members and to phosphorylate SUFU for nuclear accumulation of GLI. Hedgehog signaling activation leads to GLI-dependent transcriptional activation of target genes, such as GLI1, PTCH1, CCND2, FOXL1, JAG2 and SFRP1. GLI1-dependent positive feedback loop combined with PTCH1-dependent negative feedback loop gives rise to transient proliferation of Hedgehog target cells. Iguana homologs (DZIP1 and DZIP1L) and Costal-2 homologs (KIF7 and KIF27) are identified by comparative integromics. SHH-dependent parietal cell proliferation is implicated in gastric mucosal repair during chronic Helicobacter pylori infection. BMP-RUNX3 signaling induces IHH expression in surface differentiated epithelial cells of stomach and intestine. Hedgehog signals from epithelial cells then induces FOXL1-mediated BMP4 upregulation in mesenchymal cells. Hedgehog signaling is frequently activated in esophageal cancer, gastric cancer and pancreatic cancer due to transcriptional upregulation of Hedgehog ligands and epigenetic silencing of HHIP1/HHIP gene, encoding the Hedgehog inhibitor. However, Hedgehog signaling is rarely activated in colorectal cancer due to negative regulation by the canonical WNT signaling pathway. Hedgehog signaling molecules or targets, such as SHH, IHH, HHIP1, PTCH1 and GLI1, are applied as biomarkers for cancer diagnostics, prognostics and therapeutics. Small-molecule inhibitors for SMO or STK36 are suitable to be used for treatment of Hedgehog-dependent cancer. - Source: PubMed
Katoh YurikoKatoh Masaru