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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.


ShK, CARKL, sedoheptulokinase
The protein encoded by this gene has weak homology to several carbohydrate kinases, a class of proteins involved in the phosphorylation of sugars as they enter a cell, inhibiting return across the cell membrane. Sequence variation between this novel gene and known carbohydrate kinases suggests the possibility of a different substrate, cofactor or changes in kinetic properties distinguishing it from other carbohydrate kinases. The gene resides in a region commonly deleted in cystinosis patients, suggesting a role as a modifier for the cystinosis phenotype. The genomic region is also rich in Alu repetitive sequences, frequently involved in chromosomal rearrangements. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Kv1.3, ACID, HAD, CAN, Kv1.1
Papers on ShK
Designer and natural peptide toxin blockers of the KcsA potassium channel identified by phage display.
Goldstein et al., Ramat Gan, Israel. In Proc Natl Acad Sci U S A, Jan 2016
A phage-display strategy is presented whereby ∼1.5 million novel and natural peptides are fabricated on the scaffold present in ShK, a sea anemone type I (SAK1) toxin stabilized by three disulfide bonds.
Structural Dynamics of the Potassium Channel Blocker ShK: SRLS Analysis of (15)N Relaxation.
Chill et al., Ramat Gan, Israel. In J Phys Chem B, Jan 2016
The 35-residue ShK peptide binds with high affinity to voltage-gated potassium channels.
Discovery of variant infectious salmon anaemia virus (ISAV) of European genotype in British Columbia, Canada.
Kibenge et al., Charlottetown, Canada. In Virol J, Dec 2015
METHODS: In this study, we tested 1,106 fish tissue samples collected from (i) market-bought farmed salmonids and (ii) wild salmon from throughout British Columbia (BC), Canada, for ISAV using real time RT-qPCR targeting segment 8 and/or conventional RT-PCR with segment 8 primers and segment 6 HPR primers, and by virus isolation attempts using Salmon head kidney (SHK-1 and ASK-2) cell line monolayers.
[Effect of Kv1.3 and KCa3.1 potassium ion channels on the proliferation and migration of monocytes/macrophages].
DU et al., Zhengzhou, China. In Sheng Li Xue Bao, Nov 2015
The results showed that the recruitment of Ly-6C(hi) monocyte induced by monocytes/macrophages was suppressed by the potent Kv1.3 blocker Stichodactyla helianthus neurotoxin (ShK) or the specific KCa3.1 inhibitor TRAM-34.
Red Light Modulates Ultraviolet-Induced Gene Expression in the Epidermis of Hairless Mice.
Lanzafame et al., Moscow, Russia. In Photomed Laser Surg, Oct 2015
MATERIALS AND METHODS: The effects of 670 nm light-emitting diode (LED) array irradiation were investigated in a hairless SHK-1 mouse epidermis model.
Pharmaceutical Optimization of Peptide Toxins for Ion Channel Targets: Potent, Selective, and Long-Lived Antagonists of Kv1.3.
Miranda et al., Cambridge, United States. In J Med Chem, Oct 2015
We applied whole-molecule, brute-force, structure-activity analoging to ShK, a peptide toxin from the sea anemone Stichodactyla helianthus that inhibits the voltage-gated potassium ion channel Kv1.3, to effectively discover critical structural changes for 15× selectivity against the closely related neuronal ion channel Kv1.1.
Kv1.3 channel blockade enhances the phagocytic function of RAW264.7 macrophages.
Cao et al., Beijing, China. In Sci China Life Sci, Sep 2015
We found that blocking of the Kv1.3 channel with 100 pmol L(-1) Stichodactyla helianthus neurotoxin (ShK) enhanced the phagocytic capacities of both resting and lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages in the chicken erythrocyte system.
Computational approaches for designing potent and selective analogs of peptide toxins as novel therapeutics.
Norton et al., Sydney, Australia. In Future Med Chem, 2014
We describe ShK and HsTX1 toxins, high-affinity blockers of the voltage-gated potassium channel Kv1.3, which could be developed as therapeutic agents for autoimmune diseases.
Computational studies of marine toxins targeting ion channels.
Kuyucak et al., Sydney, Australia. In Mar Drugs, 2013
Detailed examples from the potassium channel toxins-ShK from sea anemone and κ-conotoxin PVIIA-are provided to demonstrate capabilities of the computational methods to give accurate descriptions of the channel-toxin complexes and the energetics of their binding.
The sedoheptulose kinase CARKL directs macrophage polarization through control of glucose metabolism.
Wagner et al., Vienna, Austria. In Cell Metab, 2012
CARKL-dependent metabolic reprogramming is required for proper M1- and M2-like macrophage polarization
Polarizing macrophages through reprogramming of glucose metabolism.
Jones et al., Montréal, Canada. In Cell Metab, 2012
(2012) show that the sedoheptulose kinase CARKL is required for metabolic reprogramming in activated macrophages and provide evidence that changes in glucose metabolism and the pentose phosphate pathway (PPP) influences macrophage polarization.
Development of a sea anemone toxin as an immunomodulator for therapy of autoimmune diseases.
Chandy et al., Irvine, United States. In Toxicon, 2012
The ShK toxin from the sea anemone Stichodactyla helianthus is a potent blocker of Kv1.3.
Analogs of the sea anemone potassium channel blocker ShK for the treatment of autoimmune diseases.
Norton et al., Houston, United States. In Inflamm Allergy Drug Targets, 2011
ShK, a 35-residue polypeptide isolated from the Caribbean sea anemone Stichodactyla helianthus, blocks Kv1.3 channels at picomolar concentrations.
Discovery and characterization of cnidarian peptide toxins that affect neuronal potassium ion channels.
Harvey et al., Havana, Cuba. In Toxicon, 2010
Examples from the first class are BgK from Bunodosoma granulifera, ShK from Stichodactyla helianthus and AsKS (or kaliseptine) from Anemonia sulcata (now A. viridis).
Imaging of effector memory T cells during a delayed-type hypersensitivity reaction and suppression by Kv1.3 channel block.
Cahalan et al., Irvine, United States. In Immunity, 2008
ShK-186, a specific Kv1.3 blocker, inhibited DTH and suppressed Tem cell enlargement and motility in inflamed tissue but had no effect on homing to or motility in lymph nodes of naive and central memory T (Tcm) cells.
Sedoheptulokinase deficiency due to a 57-kb deletion in cystinosis patients causes urinary accumulation of sedoheptulose: elucidation of the CARKL gene.
Wevers et al., Amsterdam, Netherlands. In Hum Mutat, 2008
the CARKL-encoded protein, sedoheptulokinase (SHK), is responsible for the reaction: sedoheptulose + ATP --> sedoheptulose-7-phosphate + ADP, and deletion of CARKL causes urinary accumulation of sedoheptulose and erythritol
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