目录号 | 产品详情 | 靶点 | |
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T2239 | HIV Protease Integrase | ||
Raltegravir potassium (MK 0518 potassium salt) 是一种整合酶抑制剂,用于研究 HIV 感染。 | |||
T0940 | Others | ||
Acesulfame potassium 是一种人造甜味剂,长期使用会影响认知功能,可能改变小鼠的神经代谢功能。 | |||
T1126 | Antibacterial Antibiotic | ||
Penicillin V Potassium (Phenoxymethylpenicillin potassium salt) 是一种有口服活性的抗生素。它可抑制链球菌,艰难梭菌和金黄色葡萄球菌的生长,可研究中耳炎,鼻窦炎,咽炎和扁桃体炎。 | |||
T23175 | Others | ||
Potassium phosphate monobasic 是生物测定时常用的缓冲液。它是中等浓度至高浓度的磷酸二氢钾水溶液,可用于制备磷酸盐缓冲液以及其他实验试剂。 | |||
T68006 | |||
Orilotimod potassium (APO805K1)可用于研究斑块状银屑病。 | |||
T3267 | Antibacterial Antibiotic | ||
Potassium guaiacolsulfonate hemihydrate (Potassium guaiacolsulfonate) 是一种芳香族磺酸,在医药中用作祛痰剂,可治疗急性呼吸道感染。它可松弛粘液,与其他药物合用,可治疗普通感冒、感染或过敏引起的咳嗽。 | |||
T19498 | Endogenous Metabolite | ||
p-Cresyl sulfate potassium (p-Tolyl sulfate potassium salt) 是一种尿毒症毒素,能够与原型蛋白质结合。 | |||
T5602 | Anti-infection Antibacterial Antibiotic | ||
Penicillin G potassium (Benzylpenicillin potassium) 是青霉素家族的一种速效抗生素。 | |||
T22328 | Others | ||
Ethyl potassium malonate 是琥珀酸脱氢酶的竞争性抑制剂,可作为生产丙二酸(三甲基甲硅烷基)乙酯的前体,丙二酸乙酯用于通过酰化制备 β-酮酯,并作为制备丙二酸叔丁酯的中间体。 | |||
T0215 | RAAS | ||
Losartan potassium (DuP-753 potassium) 是一种血管紧张素 II 受体 1 型(AT1)拮抗剂,能够与血管紧张素 II 与 AT1 的结合竞争,其 IC50=20 nM。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPH-01892 | ATP4A Protein, Human, Recombinant (His & Myc) | Human | E. coli | ||
The catalytic subunit of the gastric H(+)/K(+) ATPase pump which transports H(+) ions in exchange for K(+) ions across the apical membrane of parietal cells. Uses ATP as an energy source to pump H(+) ions to the gastric lumen while transporting K(+) ion from the lumen into the cell. Remarkably generates a million-fold proton gradient across the gastric parietal cell membrane, acidifying the gastric juice down to pH 1. Within a transport cycle, the transfer of a H(+) ion across the membrane is coupled to ATP hydrolysis and is associated with a transient phosphorylation that shifts the pump conformation from inward-facing (E1) to outward-facing state (E2). The release of the H(+) ion in the stomach lumen is followed by binding of K(+) ion converting the pump conformation back to the E1 state.
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TMPH-01893 | ATP4B Protein, Human, Recombinant (GST) | Human | E. coli | ||
The beta subunit of the gastric H(+)/K(+) ATPase pump which transports H(+) ions in exchange for K(+) ions across the apical membrane of parietal cells. Plays a structural and regulatory role in the assembly and membrane targeting of a functionally active pump. Within a transport cycle, the transfer of a H(+) ion across the membrane is coupled to ATP hydrolysis and is associated with a transient phosphorylation of the alpha subunit that shifts the pump conformation from inward-facing (E1) to outward-facing state (E2). Interacts with the phosphorylation domain of the alpha subunit and functions as a ratchet, stabilizing the lumenal-open E2 conformation and preventing the reverse reaction of the transport cycle.
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TMPH-01894 | ATP4B Protein, Human, Recombinant | Human | E. coli | ||
The beta subunit of the gastric H(+)/K(+) ATPase pump which transports H(+) ions in exchange for K(+) ions across the apical membrane of parietal cells. Plays a structural and regulatory role in the assembly and membrane targeting of a functionally active pump. Within a transport cycle, the transfer of a H(+) ion across the membrane is coupled to ATP hydrolysis and is associated with a transient phosphorylation of the alpha subunit that shifts the pump conformation from inward-facing (E1) to outward-facing state (E2). Interacts with the phosphorylation domain of the alpha subunit and functions as a ratchet, stabilizing the lumenal-open E2 conformation and preventing the reverse reaction of the transport cycle.
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TMPH-01889 | KCNK3 Protein, Human, Recombinant (His & Myc) | Human | in vitro E. coli expression system | ||
pH-dependent, voltage-insensitive, background potassium channel protein. Rectification direction results from potassium ion concentration on either side of the membrane. Acts as an outward rectifier when external potassium concentration is low. When external potassium concentration is high, current is inward.
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TMPH-01891 | KCNE2 Protein, Human, Recombinant (His) | Human | in vitro E. coli expression system | ||
Ancillary protein that assembles as a beta subunit with a voltage-gated potassium channel complex of pore-forming alpha subunits. Modulates the gating kinetics and enhances stability of the channel complex. Assembled with KCNB1 modulates the gating characteristics of the delayed rectifier voltage-dependent potassium channel KCNB1. Associated with KCNH2/HERG is proposed to form the rapidly activating component of the delayed rectifying potassium current in heart (IKr). May associate with KCNQ2 and/or KCNQ3 and modulate the native M-type current. May associate with HCN1 and HCN2 and increase potassium current. Interacts with KCNQ1; forms a heterooligomer complex leading to currents with an apparently instantaneous activation, a rapid deactivation process and a linear current-voltage relationship and decreases the amplitude of the outward current.
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TMPH-01358 | FXYD3 Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Associates with and regulates the activity of the sodium/potassium-transporting ATPase (NKA) which transports Na(+) out of the cell and K(+) into the cell. Reduces glutathionylation of the NKA beta-1 subunit ATP1B1, thus reversing glutathionylation-mediated inhibition of ATP1B1. Induces a hyperpolarization-activated chloride current when expressed in Xenopus oocytes.; Decreases the apparent K+ and Na+ affinity of the sodium/potassium-transporting ATPase over a large range of membrane potentials.; Decreases the apparent K+ affinity of the sodium/potassium-transporting ATPase only at slightly negative and positive membrane potentials and increases the apparent Na+ affinity over a large range of membrane potentials.
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TMPH-01890 | KCNA1 Protein, Human, Recombinant (His) | Human | E. coli | ||
Voltage-gated potassium channel that mediates transmembrane potassium transport in excitable membranes, primarily in the brain and the central nervous system, but also in the kidney. Contributes to the regulation of the membrane potential and nerve signaling, and prevents neuronal hyperexcitability. Forms tetrameric potassium-selective channels through which potassium ions pass in accordance with their electrochemical gradient. The channel alternates between opened and closed conformations in response to the voltage difference across the membrane. Can form functional homotetrameric channels and heterotetrameric channels that contain variable proportions of KCNA1, KCNA2, KCNA4, KCNA5, KCNA6, KCNA7, and possibly other family members as well; channel properties depend on the type of alpha subunits that are part of the channel. Channel properties are modulated by cytoplasmic beta subunits that regulate the subcellular location of the alpha subunits and promote rapid inactivation of delayed rectifier potassium channels. In vivo, membranes probably contain a mixture of heteromeric potassium channel complexes, making it difficult to assign currents observed in intact tissues to any particular potassium channel family member. Homotetrameric KCNA1 forms a delayed-rectifier potassium channel that opens in response to membrane depolarization, followed by slow spontaneous channel closure. In contrast, a heterotetrameric channel formed by KCNA1 and KCNA4 shows rapid inactivation. Regulates neuronal excitability in hippocampus, especially in mossy fibers and medial perforant path axons, preventing neuronal hyperexcitability. Response to toxins that are selective for KCNA1, respectively for KCNA2, suggests that heteromeric potassium channels composed of both KCNA1 and KCNA2 play a role in pacemaking and regulate the output of deep cerebellar nuclear neurons. May function as down-stream effector for G protein-coupled receptors and inhibit GABAergic inputs to basolateral amygdala neurons. May contribute to the regulation of neurotransmitter release, such as gamma-aminobutyric acid (GABA) release. Plays a role in regulating the generation of action potentials and preventing hyperexcitability in myelinated axons of the vagus nerve, and thereby contributes to the regulation of heart contraction. Required for normal neuromuscular responses. Regulates the frequency of neuronal action potential firing in response to mechanical stimuli, and plays a role in the perception of pain caused by mechanical stimuli, but does not play a role in the perception of pain due to heat stimuli. Required for normal responses to auditory stimuli and precise location of sound sources, but not for sound perception. The use of toxins that block specific channels suggest that it contributes to the regulation of the axonal release of the neurotransmitter dopamine. Required for normal postnatal brain development and normal proliferation of neuronal precursor cells in the brain. Plays a role in the reabsorption of Mg(2+) in the distal convoluted tubules in the kidney and in magnesium ion homeostasis, probably via its effect on the membrane potential.
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TMPH-01714 | CHRM1 Protein, Human, Recombinant (His) | Human | E. coli | ||
The muscarinic acetylcholine receptor mediates various cellular responses, including inhibition of adenylate cyclase, breakdown of phosphoinositides and modulation of potassium channels through the action of G proteins. Primary transducing effect is Pi turnover.
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TMPH-01716 | CHRM3 Protein, Human, Recombinant (B2M & His) | Human | E. coli | ||
The muscarinic acetylcholine receptor mediates various cellular responses, including inhibition of adenylate cyclase, breakdown of phosphoinositides and modulation of potassium channels through the action of G proteins. Primary transducing effect is Pi turnover.
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TMPH-01717 | CHRM5 Protein, Human, Recombinant (His) | Human | E. coli | ||
The muscarinic acetylcholine receptor mediates various cellular responses, including inhibition of adenylate cyclase, breakdown of phosphoinositides and modulation of potassium channels through the action of G proteins. Primary transducing effect is Pi turnover.
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TMPY-03615 | CSEN Protein, Human, Recombinant (His) | Human | E. coli | ||
KCNIP3 (Potassium Voltage-Gated Channel Interacting Protein 3, also known as CSEN) is a Protein Coding gene. CSEN is a member of the family of voltage-gated potassium (Kv) channel-interacting proteins, which belong to the recoverin branch of the EF-hand superfamily. Members of this family are integral subunit components of native Kv4 channel complexes that may regulate A-type currents, and hence neuronal excitability, in response to changes in intracellular calcium. CSEN also functions as a calcium-regulated transcriptional repressor and interacts with presenilins. CSEN binds to the DRE element of genes including PDYN and FOS. CSEN is broadly expressed in the brain, thyroid, and other tissues. Diseases associated with KCNIP3 include Alzheimer's Disease and Niemann-Pick Disease, Type C2.
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TMPH-02309 | KCNAB2 Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Cytoplasmic potassium channel subunit that modulates the characteristics of the channel-forming alpha-subunits. Contributes to the regulation of nerve signaling, and prevents neuronal hyperexcitability. Promotes expression of the pore-forming alpha subunits at the cell membrane, and thereby increases channel activity. Promotes potassium channel closure via a mechanism that does not involve physical obstruction of the channel pore. Promotes KCNA4 channel closure. Modulates the functional properties of KCNA5. Enhances KCNB2 channel activity. Binds NADPH and has NADPH-dependent aldoketoreductase activity. Has broad substrate specificity and can catalyze the reduction of methylglyoxal, 9,10-phenanthrenequinone, prostaglandin J2, 4-nitrobenzaldehyde, 4-nitroacetophenone and 4-oxo-trans-2-nonenal (in vitro).
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TMPH-01715 | CHRM2 Protein, Human, Recombinant (His) | Human | E. coli | ||
The muscarinic acetylcholine receptor mediates various cellular responses, including inhibition of adenylate cyclase, breakdown of phosphoinositides and modulation of potassium channels through the action of G proteins. Primary transducing effect is adenylate cyclase inhibition. Signaling promotes phospholipase C activity, leading to the release of inositol trisphosphate (IP3); this then triggers calcium ion release into the cytosol.
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TMPJ-00652 | PSD-95 Protein, Rat, Recombinant (His) | Rat | E. coli | ||
Disks large homolog 4(DLG4) is a cell membrane protein and it is a member of the membrane-associated guanylate kinase (MAGUK) family. The protein contains 1 guanylate kinase-like domain,3 PDZ (DHR) domains and 1 SH3 domain. With PSD-93 it is recruited into the same NMDA receptor and potassium channel clusters. These two MAGUK proteins may interact at postsynaptic sites to form a multimeric scaffold for the clustering of receptors, ion channels, and associated signaling proteins. DLG4 is the best studied member of the MAGUK-family of PDZ domain-containing proteins. Like all MAGUK-family proteins, its basic structure includes three PDZ domains, an SH3 domain, and a guanylate kinase-like domain (GK) connected by disordered linker regions. It is almost exclusively located in the post synaptic density of neurons, and is involved in anchoring synaptic proteins. Its direct and indirect binding partners include neuroligin, NMDA receptors, AMPA receptors, and potassium channels.
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TMPY-01854 | DPP10 Protein, Human, Recombinant (His) | Human | HEK293 | ||
Inactive dipeptidyl peptidase 1, also known as Dipeptidyl peptidase IV-related protein 3, Dipeptidyl peptidase X, Dipeptidyl peptidase-like protein 2, DPRP-3, DPL2 and DPP1, is a single-pass type II membrane protein which belongs to thepeptidase S9B family.DPPIV subfamily. It may modulate cell surface expression and activity of the potassium channels KCND1 and KCND2. DPP1 / DPRP3 has no detectable protease activity, most likely due to the absence of the conserved serine residue normally present in the catalytic domain of serine proteases. However, it does bind specific voltage-gated potassium channels and alters their expression and biophysical properties. Genetic variations in DPP1 are associated with susceptibility to asthma (ASTHMA). The most common chronic disease affecting children and young adults. It is a complex genetic disorder with a heterogeneous phenotype, largely attributed to the interactions among many genes and between these genes and the environment. It is characterized by recurrent attacks of paroxysmal dyspnea, with weezing due to spasmodic contraction of the bronchi.
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TMPH-01609 | LGI1 Protein, Human, Recombinant (His & Myc) | Human | E. coli | ||
Regulates voltage-gated potassium channels assembled from KCNA1, KCNA4 and KCNAB1. It slows down channel inactivation by precluding channel closure mediated by the KCNAB1 subunit. Ligand for ADAM22 that positively regulates synaptic transmission mediated by AMPA-type glutamate receptors. Plays a role in suppressing the production of MMP1/3 through the phosphatidylinositol 3-kinase/ERK pathway. May play a role in the control of neuroblastoma cell survival.
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TMPJ-00988 | SEPHS1 Protein, Human, Recombinant (His) | Human | Human Cells | ||
Selenophosphate synthetase 1 (SEPHS1) belongs to the selenophosphate synthase 1 family, Class II subfamily. It has four different isoforms by alternative splicing. Isoform 1 and isoform 2 are gradually expressed during the cell cycle until G2/M phase and then decreased, which Isoform 3 is gradually expressed during the cell cycle until S phase and then decreased. SEPHS1 can be activated by phosphate ions and by potassium ions. It can synthesize synthesizes selenophosphate from selenide and ATP. Selenophosphate is the selenium donor used to synthesize selenocysteine, which is co-translationally incorporated into selenoproteins at in-frame UGA codons.
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TMPH-01745 | NOX4 Protein, Human, Recombinant (Cell-Free, His) | Human | in vitro E. coli expression system | ||
Constitutive NADPH oxidase which generates superoxide intracellularly upon formation of a complex with CYBA/p22phox. Regulates signaling cascades probably through phosphatases inhibition. May function as an oxygen sensor regulating the KCNK3/TASK-1 potassium channel and HIF1A activity. May regulate insulin signaling cascade. May play a role in apoptosis, bone resorption and lipolysaccharide-mediated activation of NFKB. May produce superoxide in the nucleus and play a role in regulating gene expression upon cell stimulation. Isoform 3 is not functional. Isoform 5 and isoform 6 display reduced activity.; Involved in redox signaling in vascular cells. Constitutively and NADPH-dependently generates reactive oxygen species (ROS). Modulates the nuclear activation of ERK1/2 and the ELK1 transcription factor, and is capable of inducing nuclear DNA damage. Displays an increased activity relative to isoform 1.
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TMPH-01372 | GJA1 Protein, Human, Recombinant (His) | Human | E. coli | ||
Gap junction protein that acts as a regulator of bladder capacity. A gap junction consists of a cluster of closely packed pairs of transmembrane channels, the connexons, through which materials of low MW diffuse from one cell to a neighboring cell. May play a critical role in the physiology of hearing by participating in the recycling of potassium to the cochlear endolymph. Negative regulator of bladder functional capacity: acts by enhancing intercellular electrical and chemical transmission, thus sensitizing bladder muscles to cholinergic neural stimuli and causing them to contract. May play a role in cell growth inhibition through the regulation of NOV expression and localization. Plays an essential role in gap junction communication in the ventricles.
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TMPH-01746 | NOX4 Protein, Human, Recombinant (E. coli, His) | Human | E. coli | ||
Constitutive NADPH oxidase which generates superoxide intracellularly upon formation of a complex with CYBA/p22phox. Regulates signaling cascades probably through phosphatases inhibition. May function as an oxygen sensor regulating the KCNK3/TASK-1 potassium channel and HIF1A activity. May regulate insulin signaling cascade. May play a role in apoptosis, bone resorption and lipolysaccharide-mediated activation of NFKB. May produce superoxide in the nucleus and play a role in regulating gene expression upon cell stimulation. Isoform 3 is not functional. Isoform 5 and isoform 6 display reduced activity.; Involved in redox signaling in vascular cells. Constitutively and NADPH-dependently generates reactive oxygen species (ROS). Modulates the nuclear activation of ERK1/2 and the ELK1 transcription factor, and is capable of inducing nuclear DNA damage. Displays an increased activity relative to isoform 1.
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TMPY-03491 | Lysozyme 2 Protein, Human, Recombinant (His) | Human | Baculovirus-Insect Cells | ||
The lysozyme 2 gene is a member of a family of lysozyme-like genes. Lysozymes, especially C-type lysozymes, are well-recognized bacteriolytic factors widely distributed in the animal kingdom and play a mainly protective role in host defense. Lysozymes damage bacterial cell walls by catalyzing the hydrolysis of 1,4-beta-linkages between N-acetylmuramic acid and N-acetyl-D-glucosamine residues in a peptidoglycan and between N-acetyl-D-glucosamine residues in chitodextrins. Lysozyme is part of the innate immune system. Reduced lysozyme levels have been associated with bronchopulmonary dysplasia in newborns. In certain cancers (especially myelomonocytic leukemia) excessive production of lysozyme by cancer cells can lead to toxic levels of lysozyme in the blood. High lysozyme blood levels can lead to kidney failure and low blood potassium, conditions that may improve or resolve with treatment of the primary malignancy.
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TMPY-02737 | DPP2 Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
DPP7 (dipeptidylpeptidase 7), also known as DPPII and DPP2, is a post-proline cleaving aminopeptidase expressed in quiescent lymphocytes. Dipeptidyl peptidases (DPPs) have post-proline dipeptidyl aminopeptidase activity, cleaving Xaa-Pro dipeptides from the N-termini of proteins. DPPs mediate regulatory activity of their substrates and have been linked to a variety of diseases including type 2 diabetes, obesity and cancer. DPPs can bind specific voltage-gated potassium channels and alter their expression and biophysical properties and may also influence T cells. DPP proteins include DPRP1, DPRP2, DPP3, DPP7, DPP10, DPPX and CD26. It localizes to lysosomes. DPP7 localizes to lysosomes and exists as a homodimer via its leucine zipper motif and is involved in the degradation of oligopeptides. In response to calcium release, it can be secreted in its active form. It is essential for lymphocyte survival, as the inhibition of DPP7 results in quiescent cell apoptosis.
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TMPY-00777 | DPP2 Protein, Human, Recombinant (His) | Human | HEK293 | ||
DPP7 (dipeptidylpeptidase 7), also known as DPPII and DPP2, is a post-proline cleaving aminopeptidase expressed in quiescent lymphocytes. Dipeptidyl peptidases (DPPs) have post-proline dipeptidyl aminopeptidase activity, cleaving Xaa-Pro dipeptides from the N-termini of proteins. DPPs mediate regulatory activity of their substrates and have been linked to a variety of diseases including type 2 diabetes, obesity and cancer. DPPs can bind specific voltage-gated potassium channels and alter their expression and biophysical properties and may also influence T cells. DPP proteins include DPRP1, DPRP2, DPP3, DPP7, DPP10, DPPX and CD26. It localizes to lysosomes. DPP7 localizes to lysosomes and exists as a homodimer via its leucine zipper motif and is involved in the degradation of oligopeptides. In response to calcium release, it can be secreted in its active form. It is essential for lymphocyte survival, as the inhibition of DPP7 results in quiescent cell apoptosis.
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TMPY-01695 | CASPR2 Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
CNTNAP2/CASPR2 is a member of the neurexin family which functions in the vertebrate nervous system as cell adhesion molecules and receptors. This protein, like other neurexin proteins, contains epidermal growth factor repeats and laminin G domains. In addition, it includes an F5/8 type C domain, discoidin/neuropilin- and fibrinogen-like domains, thrombospondin N-terminal-like domains and a putative PDZ binding site. CNTNAP2/CASPR2 is localized at the juxtaparanodes of myelinated axons, and mediates interactions between neurons and glia during nervous system development and is also involved in localization of potassium channels within differentiating axons. This protein encoding gene is directly bound and regulated by forkhead box protein P2 (FOXP2), a transcription factor related to speech and language development. This gene has been implicated in multiple neurodevelopmental disorders, including Gilles de la Tourette syndrome, schizophrenia, epilepsy, autism, ADHD and mental retardation. CNTNAP2/CASPR2 may play a role in the formation of functional distinct domains critical for saltatory conduction of nerve impulses in myelinated nerve fibers. CNTNAP2/CASPR2 Seems to demarcate the juxtaparanodal region of the axo-glial junction.
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TMPH-01028 | KCNMA1 Protein, Human, Recombinant | Human | E. coli | ||
Potassium channel activated by both membrane depolarization or increase in cytosolic Ca(2+) that mediates export of K(+). It is also activated by the concentration of cytosolic Mg(2+). Its activation dampens the excitatory events that elevate the cytosolic Ca(2+) concentration and/or depolarize the cell membrane. It therefore contributes to repolarization of the membrane potential. Plays a key role in controlling excitability in a number of systems, such as regulation of the contraction of smooth muscle, the tuning of hair cells in the cochlea, regulation of transmitter release, and innate immunity. In smooth muscles, its activation by high level of Ca(2+), caused by ryanodine receptors in the sarcoplasmic reticulum, regulates the membrane potential. In cochlea cells, its number and kinetic properties partly determine the characteristic frequency of each hair cell and thereby helps to establish a tonotopic map. Kinetics of KCNMA1 channels are determined by alternative splicing, phosphorylation status and its combination with modulating beta subunits. Highly sensitive to both iberiotoxin (IbTx) and charybdotoxin (CTX).
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TMPY-06599 | ATP1B4 Protein, Human, Recombinant (His) | Human | E. coli | ||
ATP1B4 is a member of the X(+)/potassium ATPases subunit beta family. It is highly expressed in skeletal muscle and at a lower level in heart. ATP1B4 gene can be found in all vertebrate genomes sequenced to date. However, this gene has undergone a change in function in placental mammals compared to other species. Specifically, in fish, avian, and amphibian species, this gene encodes plasma membrane-bound beta-subunits of Na, K-ATPase. In placental mammals, the encoded protein interacts with the nuclear transcriptional coregulator SKIP and may be involved in the regulation of TGF-beta signaling. ATP1B4 may act as a transcriptional coregulator during muscle development through its interaction with SNW1. Na+, K+-ATPase is an important regulator of intracellular electrolyte levels in most mammalian cells. It is a Mg2+-dependent transport pump responsible for maintaining the low intracellular Na+:K+ ratio that is essential for cell homeostasis and physiological function. It catalyzes the active uptake of K+ and extrusion of Na+ at the expense of hydrolyzing ATP with a stoichiometry of 3 Na+ for 2 K+. ATP1B4 has lost its ancestral function as a Na,K-ATPase beta-subunit.
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TMPY-04561 | SGK3 Protein, Human, Recombinant (His & GST) | Human | Baculovirus-Insect Cells | ||
Serine / threonine-protein kinase Sgk3, also known as Serum / glucocorticoid-regulated kinase 3, Serum / glucocorticoid-regulated kinase-like and SGK3, is a cytoplasmic vesicle protein that belongs to the protein kinase superfamily and AGC Ser/Thr protein kinase family. SGK3 contains one AGC-kinase C-terminal domain, one protein kinase domain and one PX (phox homology) domain. Two specific sites of SGK3, one in the kinase domain (Thr-32) and the other in the C-terminal regulatory region (Ser-486), is needed to be phosphorylated for its full activation. SGK3 is expressed in most tissues with highest levels in pancreas, kidney liver, heart and brain and lower levels in lung, placenta and skeletal muscle. SGK3 is involved in the activation of potassium channels. It mediates cell IL-3-dependent survival signals. SGK3 participates in the regulation of HERG by increasing HERG protein abundance in the plasma membrane and may thus modify the duration of the cardiac action potential. SGK3 is also a very important and characteristic molecule that plays a critical role in both hair follicle morphogenesis and hair cycling.
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TMPH-00818 | Delta-theraphotoxin-Hm1a Protein, Heteroscodra maculata, Recombinant (His & Myc & SUMO) | Heteroscodra maculata | E. coli | ||
Gating-modifier toxin that potently inhibits inactivation of the mammalian Nav1.1/SCN1A sodium channel (EC(50)=38 nM). Also moderately inhibits inactivation of Nav1.2/SCN2A (EC(50)=236 nM) and Nav1.3/SCN3A (EC(50)=220 nM) when the channels are expressed in oocytes without the beta-1 auxiliary subunit. Does not inhibit inactivation of Nav1.2/SCN2A when the channel is coexpressed with the beta-1 auxiliary subunit. When tested on Nav1.1/SCN1A channel, it enhances peak current amplitude and potently delays channel inactivation in a dose-dependent manner, leading to a large sustained current. It has no effect on the voltage-dependence of steady-state activation, and induces a depolarizing shift in the voltage dependence of inactivation. In addition, it does not modify the recovery from fast inactivation in Nav1.1/SCN1A. The binding affinity and subtype selectivity of the toxin towards Nav1.1/SCN1A channel is determined by residues within both the S1-S2 and S3-S4 loops of the domain IV voltage sensor of the channel. This toxin also weakly inhibits several subtypes of voltage-gated potassium channels. It moderately blocks Kv2.1/KCNB1 (23% inhibition at 100 nM), Kv2.2/KCNB2 (19.7% at 100 nM and 51% at 300 nM), Kv4.1/KCND1 (IC(50)=280 nM), Kv4.2/KCND2 (39% at 300 nM) and Kv4.3/KCND3 (43% at 300 nM). In vivo, intracerebroventricular injection into mice elicits convulsions, spasms, tremors and rapid death. When injected into mouse hindpaw, the toxin elicits an immediate and robust response to pain. However, intraplantar injection of toxin does not cause neurogenic inflammation or alter sensitivity to heat, indicative of a modality-specific effect on mechanosensitive neurons. In Dravet syndrome mice model, intracerebroventricular infusion of this peptide rescues mice from seizures and premature death.
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TMPH-02521 | PYCARD Protein, Mouse, Recombinant (His & Myc) | Mouse | E. coli | ||
Functions as key mediator in apoptosis and inflammation. Promotes caspase-mediated apoptosis involving predominantly caspase-8 and also caspase-9 in a probable cell type-specific manner. Involved in activation of the mitochondrial apoptotic pathway, promotes caspase-8-dependent proteolytic maturation of BID independently of FADD in certain cell types and also mediates mitochondrial translocation of BAX and activates BAX-dependent apoptosis coupled to activation of caspase-9, -2 and -3. Involved in macrophage pyroptosis, a caspase-1-dependent inflammatory form of cell death and is the major constituent of the ASC pyroptosome which forms upon potassium depletion and rapidly recruits and activates caspase-1. In innate immune response believed to act as an integral adapter in the assembly of the inflammasome which activates caspase-1 leading to processing and secretion of proinflammatory cytokines. The function as activating adapter in different types of inflammasomes is mediated by the pyrin and CARD domains and their homotypic interactions. Required for recruitment of caspase-1 to inflammasomes containing certain pattern recognition receptors, such as NLRP2, NLRP3, AIM2 and probably IFI16. In the NLRP1 and NLRC4 inflammasomes seems not be required but facilitates the processing of procaspase-1. In cooperation with NOD2 involved in an inflammasome activated by bacterial muramyl dipeptide leading to caspase-1 activation. May be involved in DDX58-triggered proinflammatory responses and inflammasome activation. In collaboration with AIM2 which detects cytosolic double-stranded DNA may also be involved in a caspase-1-independent cell death that involves caspase-8. In adaptive immunity may be involved in maturation of dendritic cells to stimulate T-cell immunity and in cytoskeletal rearrangements coupled to chemotaxis and antigen uptake may be involved in post-transcriptional regulation of the guanine nucleotide exchange factor DOCK2; the latter function is proposed to involve the nuclear form. Also involved in transcriptional activation of cytokines and chemokines independent of the inflammasome; this function may involve AP-1, NF-kappa-B, MAPK and caspase-8 signaling pathways. For regulation of NF-kappa-B activating and inhibiting functions have been reported. Modulates NF-kappa-B induction at the level of the IKK complex by inhibiting kinase activity of CHUK and IKBK. Proposed to compete with RIPK2 for association with CASP1 thereby down-regulating CASP1-mediated RIPK2-dependent NF-kappa-B activation and activating interleukin-1 beta processing. Modulates host resistance to DNA virus infection, probably by inducing the cleavage of and inactivating CGAS in presence of cytoplasmic double-stranded DNA.
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TMPH-01719 | OPRM1 Protein, Human, Recombinant (His) | Human | in vitro E. coli expression system | ||
Receptor for endogenous opioids such as beta-endorphin and endomorphin. Receptor for natural and synthetic opioids including morphine, heroin, DAMGO, fentanyl, etorphine, buprenorphin and methadone. Agonist binding to the receptor induces coupling to an inactive GDP-bound heterotrimeric G-protein complex and subsequent exchange of GDP for GTP in the G-protein alpha subunit leading to dissociation of the G-protein complex with the free GTP-bound G-protein alpha and the G-protein beta-gamma dimer activating downstream cellular effectors. The agonist- and cell type-specific activity is predominantly coupled to pertussis toxin-sensitive G(i) and G(o) G alpha proteins, GNAI1, GNAI2, GNAI3 and GNAO1 isoforms Alpha-1 and Alpha-2, and to a lesser extent to pertussis toxin-insensitive G alpha proteins GNAZ and GNA15. They mediate an array of downstream cellular responses, including inhibition of adenylate cyclase activity and both N-type and L-type calcium channels, activation of inward rectifying potassium channels, mitogen-activated protein kinase (MAPK), phospholipase C (PLC), phosphoinositide/protein kinase (PKC), phosphoinositide 3-kinase (PI3K) and regulation of NF-kappa-B. Also couples to adenylate cyclase stimulatory G alpha proteins. The selective temporal coupling to G-proteins and subsequent signaling can be regulated by RGSZ proteins, such as RGS9, RGS17 and RGS4. Phosphorylation by members of the GPRK subfamily of Ser/Thr protein kinases and association with beta-arrestins is involved in short-term receptor desensitization. Beta-arrestins associate with the GPRK-phosphorylated receptor and uncouple it from the G-protein thus terminating signal transduction. The phosphorylated receptor is internalized through endocytosis via clathrin-coated pits which involves beta-arrestins. The activation of the ERK pathway occurs either in a G-protein-dependent or a beta-arrestin-dependent manner and is regulated by agonist-specific receptor phosphorylation. Acts as a class A G-protein coupled receptor (GPCR) which dissociates from beta-arrestin at or near the plasma membrane and undergoes rapid recycling. Receptor down-regulation pathways are varying with the agonist and occur dependent or independent of G-protein coupling. Endogenous ligands induce rapid desensitization, endocytosis and recycling whereas morphine induces only low desensitization and endocytosis. Heterooligomerization with other GPCRs can modulate agonist binding, signaling and trafficking properties. Involved in neurogenesis. Isoform 12 couples to GNAS and is proposed to be involved in excitatory effects. Isoform 16 and isoform 17 do not bind agonists but may act through oligomerization with binding-competent OPRM1 isoforms and reduce their ligand binding activity.
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