目录号 | 产品详情 | 靶点 | |
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T78521 | Others | ||
Mc-Alanyl-Alanyl-Asparagine-PAB-MMAE(化合物S6)作为抗肿瘤微环境特异性活化的抗癌剂,已被证实能够抑制小鼠肿瘤生长。 | |||
T2O2731 | Others Endogenous Metabolite | ||
L-Aspartic acid (Aspatofort) 是一种氨基酸,是结肠特异性药物输送的前体药物。 | |||
TP1771 | |||
NGR peptide Trifluoroacetate containing the asparagine-glycine-arginine (NGR) motif is recognized by CD13/aminopeptidase N (APN) receptor isoforms that are selectively overexpressed in tumor neovasculature. | |||
T69056 | |||
Albizziin is amino acid analog which acts as a competitive inhibitor of asparagine synthetase with respect to glutamine. Albizziin has been used to isolate mutants of Chinese hamster ovary cells with alterations in levels of the target enzyme. Several classes of mutations can be distinguished on the basis of cross-resistance to beta-aspartyl hydroxamate, another amino acid analog. Studies on asparagine synthetase indicate that resistance to albizziin may be due to altered regulation of asparagine synthetase, structural mutations of the enzyme, and gene amplification. | |||
T38116 | |||
Fmoc-Ala-Glu-Asn-Lys-NH2 is a peptide inhibitor that selectively targets asparagine endopeptidase (AEP) and inhibits the cleavage of amyloid precursor protein (APP). AEP, a pH-controlled cysteine proteinase, plays a crucial role in the proteolytic processing of APP, and its activity is enhanced during the aging process [1]. | |||
T65016 | |||
Bleomycin A2,作为一种抗肿瘤抗生素,能促进DNA降解,同时也是一种天冬氨酸/天冬酰胺-β-羟化酶(AspH)的抑制剂,其IC50为1.47 μM。 | |||
T75412 | |||
Peptide-N-Glycosidase F (PNGaseF) 是一种天冬酰胺酰胺酶。Peptide-N-Glycosidase F 催化来自糖蛋白的高甘露糖、杂合和复杂寡糖的内层 GlcNAc 和天冬酰胺残基之间的 N-连接寡糖裂解。Peptide-N-Glycosidase F 可用于糖蛋白的结构和功能研究。 | |||
T69829 | |||
GCN2iB is a GCN2 inhibitor. GCN2iB may be useful for the treatment of cancer. The inhibition of GCN2 sensitizes cancer cells with low basal-level expression of asparagine synthetase (ASNS) to the antileukemic agent L-asparaginase (ASNase) in vitro and in vivo. | |||
T61004 | |||
APE-IN-1 可用于阿尔茨海默病的早期诊断和药物研发。APE-IN-1 是一种有效的天冬酰胺内肽酶(APE) 抑制剂,IC50值为 89 nM。 | |||
T83506 | |||
[Asn23]-beta-Amyloid (1-42), iowa mutation 是具有生物活性的肽,与阿尔茨海默病中的一种严重神经病理状况——大脑淀粉样蛋白血管病 (CAA) 密切相关。这种变异是由于在 APP 694 位点发生了错义突变,其中 Asp 23 被 Asn 取代,导致的。该变异形式的β-淀粉样肽倾向于更快聚集,形成具有毒性的原纤维。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPH-00514 | Endo H Protein, Streptomyces plicatus, Recombinant (His) | Streptomyces plicatus | Yeast | ||
Cleaves asparagine-linked oligomannose and hybrid, but not complex, oligosaccharides from glycoproteins.
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TMPH-01598 | CCBL2 Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Catalyzes the irreversible transamination of the L-tryptophan metabolite L-kynurenine to form kynurenic acid (KA), an intermediate in the tryptophan catabolic pathway which is also a broad spectrum antagonist of the three ionotropic excitatory amino acid receptors among others. May catalyze the beta-elimination of S-conjugates and Se-conjugates of L-(seleno)cysteine, resulting in the cleavage of the C-S or C-Se bond. Has transaminase activity towards L-kynurenine, tryptophan, phenylalanine, serine, cysteine, methionine, histidine, glutamine and asparagine with glyoxylate as an amino group acceptor (in vitro). Has lower activity with 2-oxoglutarate as amino group acceptor (in vitro).
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TMPY-02050 | DDOST Protein, Human, Recombinant | Human | E. coli | ||
The enzyme oligosaccharyltransferase (dolichyl-diphosphooligosaccharide-protein glycosyltransferase) (DDOST), or 48-kDa subunit (OST48) is one of the catalytic subunits in this complex, exerts a typical type I membrane topology, containing a large luminal domain, a hydrophobic transmembrane domain and a short cytosolic peptide tail. DDOST/OST48 catalyzes the transfer of a high-mannose oligosaccharide (GlcNac2Man9Glc3) from a dolichol-linked oligosaccharide donor (dolichol-P-GlcNac2Man9Glc3) onto the asparagine acceptor site within an Asn-X-Ser/Thr consensus motif in nascent polypeptide chains across the membrane of the endoplasmic reticulum. The mammalian oligosaccharyltransferase (OST) is an oligomeric complex composed of three type I transmembrane proteins of the endoplasmic reticulum: ribophorin I (RI), ribophorin II (RII), and OST48. OST48 is not a glycoprotein and is not recognized by antibodies to either ribophorin. Like ribophorins I and II, OST48 was found to be an integral membrane protein, with the majority of the polypeptide located within the lumen of the endoplasmic reticulum (ER). OST48 does not show significant amino acid sequence homology to either ribophorin I or II. It had been found that only the luminal domain of RI contains ER retention information. The dilysine motif in OST48 functions as an ER localization motif because OST48 in which the two lysine residues are replaced by serine (OST48ss) is no longer retained in the ER and is found instead also at the plasma membrane.
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TMPH-03274 | ATF-4 Protein, Rat, Recombinant (His & Myc) | Rat | E. coli | ||
Transcription factor that binds the cAMP response element (CRE) (consensus: 5'-GTGACGT[AC][AG]-3') and displays two biological functions, as regulator of metabolic and redox processes under normal cellular conditions, and as master transcription factor during integrated stress response (ISR). Binds to asymmetric CRE's as a heterodimer and to palindromic CRE's as a homodimer. Core effector of the ISR, which is required for adaptation to various stress such as endoplasmic reticulum (ER) stress, amino acid starvation, mitochondrial stress or oxidative stress. During ISR, ATF4 translation is induced via an alternative ribosome translation re-initiation mechanism in response to EIF2S1/eIF-2-alpha phosphorylation, and stress-induced ATF4 acts as a master transcription factor of stress-responsive genes in order to promote cell recovery. Promotes the transcription of genes linked to amino acid sufficiency and resistance to oxidative stress to protect cells against metabolic consequences of ER oxidation. Activates the transcription of NLRP1, possibly in concert with other factors in response to ER stress. Activates the transcription of asparagine synthetase (ASNS) in response to amino acid deprivation or ER stress. However, when associated with DDIT3/CHOP, the transcriptional activation of the ASNS gene is inhibited in response to amino acid deprivation. Together with DDIT3/CHOP, mediates programmed cell death by promoting the expression of genes involved in cellular amino acid metabolic processes, mRNA translation and the terminal unfolded protein response (terminal UPR), a cellular response that elicits programmed cell death when ER stress is prolonged and unresolved. Together with DDIT3/CHOP, activates the transcription of the IRS-regulator TRIB3 and promotes ER stress-induced neuronal cell death by regulating the expression of BBC3/PUMA in response to ER stress. May cooperate with the UPR transcriptional regulator QRICH1 to regulate ER protein homeostasis which is critical for cell viability in response to ER stress. In the absence of stress, ATF4 translation is at low levels and it is required for normal metabolic processes such as embryonic lens formation, fetal liver hematopoiesis, bone development and synaptic plasticity. Acts as a regulator of osteoblast differentiation in response to phosphorylation by RPS6KA3/RSK2: phosphorylation in osteoblasts enhances transactivation activity and promotes expression of osteoblast-specific genes and post-transcriptionally regulates the synthesis of Type I collagen, the main constituent of the bone matrix. Cooperates with FOXO1 in osteoblasts to regulate glucose homeostasis through suppression of beta-cell production and decrease in insulin production. Activates transcription of SIRT4. Regulates the circadian expression of the core clock component PER2 and the serotonin transporter SLC6A4. Binds in a circadian time-dependent manner to the cAMP response elements (CRE) in the SLC6A4 and PER2 promoters and periodically activates the transcription of these genes. Mainly acts as a transcriptional activator in cellular stress adaptation, but it can also act as a transcriptional repressor: acts as a regulator of synaptic plasticity by repressing transcription, thereby inhibiting induction and maintenance of long-term memory. Regulates synaptic functions via interaction with DISC1 in neurons, which inhibits ATF4 transcription factor activity by disrupting ATF4 dimerization and DNA-binding.
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