Rabbit Anti-Human STK36 (internal) Polyclonal antibody

Name: Rabbit Anti-Human STK36 (internal) Polyclonal antibody
SKU: DPABH-01289
Rating: 5 (1 reviews)

Rabbit Anti-Human STK36 (internal) Polyclonal antibody for WB, IHC

COA

SDS

Datasheet

Key features and details

Target: STK36
Host: Rabbit
Application: WB, IHC
Species Reactivity: Human

Summary

Specifications

Antibody Isotype

IgG

Species Reactivity

Human

Immunogen

Synthesized peptide derived from internal of human STK36.

Conjugate

Unconjugated

Applications

Application Notes

WB: 1:500-1:3000
IHC: 1:50-1:100

General Notes

This product (Catalog No. DPABH-01289) is a rabbit-derived IgG polyclonal antibody raised against human STK36. It has been affinity purified by protein A. This gene encodes a member of the serine/threonine kinase family of enzymes. This family member is similar to a Drosophila protein that plays a key role in the Hedgehog signaling pathway. This human protein is a positive regulator of the GLI zinc-finger transcription factors. Knockout studies of the homologous mouse gene suggest that defects in this human gene may lead to congenital hydrocephalus, possibly due to a functional defect in motile cilia. Because Hedgehog signaling is frequently activated in certain kinds of gastrointestinal cancers, it has been suggested that this gene is a target for the treatment of these cancers. Alternative splicing of this gene results in multiple transcript variants.
DPABH-01289 is suitable for use in Western blot (WB) (1:500–1:3,000), IHC (1:50–1:100) applications.
DPABH-01289 is supplied as a liquid formulation in PBS (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. For long-term storage, keep at −20 °C. For short-term use, store at 2–8 °C. Avoid repeated freeze–thaw cycles to maintain antibody integrity and performance.

Target

Alternative Names

Serine/threonine-protein kinase 36 EC 2.7.11.1; Fused homolog STK36

Entrez Gene ID

27148

UniProt ID

Q9NRP7

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

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References

A synthetic lethal siRNA screen identifying genes mediating sensitivity to a PARP inhibitor

EMBO JOURNAL

Authors: Turner, Nicholas C.; Lord, Christopher J.; Iorns, Elizabeth; Brough, Rachel; Swift, Sally; Elliott, Richard; Rayter, Sydonia; Tutt, Andrew N.; Ashworth, Alan

Abstract

Inhibitors of poly (ADP-ribose)-polymerase-1 (PARP) are highly lethal to cells with deficiencies in BRCA1, BRCA2 or other components of the homologous recombination pathway. This has led to PARP inhibitors entering clinical trials as a potential therapy for cancer in carriers of BRCA1 and BRCA2 mutations. To discover new determinants of sensitivity to these drugs, we performed a PARP-inhibitor synthetic lethal short interfering RNA (siRNA) screen. We identified a number of kinases whose silencing strongly sensitised to PARP inhibitor, including cyclin-dependent kinase 5 (CDK5), MAPK12, PLK3, PNKP, STK22c and STK36. How CDK5 silencing mediates sensitivity was investigated. Previously, CDK5 has been suggested to be active only in a neuronal context, but here we show that CDK5 is required in non-neuronal cells for the DNA-damage response and, in particular, intra-S and G(2)/M cell-cycle checkpoints. These results highlight the potential of synthetic lethal siRNA screens with chemical inhibitors to define new determinants of sensitivity and potential therapeutic targets.

Phosphorylation of Ci/Gli by Fused Family Kinases Promotes Hedgehog Signaling

DEVELOPMENTAL CELL

Authors: Han, Yuhong; Wang, Bing; Cho, Yong Suk; Zhu, Jian; Wu, Jiang; Chen, Yongbin; Jiang, Jin

Abstract

Hedgehog (Hh) signaling culminates in the conversion of the latent transcription factor Cubitus interruptus (Ci)/Gli into its activator form (Ci A /Gli A), but the underlying mechanism remains poorly understood. Here, we demonstrate that Hh stimulates the phosphorylation of Ci by the Ser/Thr kinase Fused (Fu) and that Fu-mediated phosphorylation of Ci promotes its activation. We find that Fu directly phosphorylates Ci on Ser218 and Ser1230, which primes its further phosphorylation by CK1 on adjacent sties. These phosphorylation events alter Ci binding to the pathway inhibitor Suppressor of fused (Sufu) and facilitate the recruitment of Transportion and the transcriptional coactivator CBP. Furthermore, we provide evidence that Sonic hedgehog (Shh) activates Gli2 by stimulating its phosphorylation on conserved sites through the Fu-family kinases ULK3 and mFu/STK36 in a manner depending on Gli2 ciliary localization. Hence, Fu-family kinase-mediated phosphorylation of Ci/Gli serves as a conserved mechanism that activates the Hh pathway transcription factor.