Hex
目录号 : GC63451
Hex 是烯醇酶 (enolase) 的抑制剂，其对 ENO2 和 ENO1 的 Ki 值分别为 74.4 nM 和 269.4 nM。
Cas No.:2004714-32-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Hex is an enolase inhibitor, with Ki values of 74.4 nM and 269.4 nM for ENO2 and ENO1, respectively[1].
[1]. BOARD OF REGENTS, et al. Enolase inhibitors and methods of treatment there with. WO2016145113A1
| Cas No. | 2004714-32-1 | SDF | |
| 分子式 | C5H10NO5P | 分子量 | 195.11 |
| 溶解度 | DMSO : 250 mg/mL (1281.33 mM; Need ultrasonic)|Methanol : 25 mg/mL (128.13 mM; Need ultrasonic) | 储存条件 | 4°C, away from moisture and light |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 5.1253 mL | 25.6266 mL | 51.2531 mL |
| 5 mM | 1.0251 mL | 5.1253 mL | 10.2506 mL |
| 10 mM | 0.5125 mL | 2.5627 mL | 5.1253 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Electromyographic Comparison of Barbell Deadlift, Hex Bar Deadlift, and Hip Thrust Exercises: A Cross-Over Study
J Strength Cond Res 2018 Mar;32(3):587-593.PMID:28151780DOI:10.1519/JSC.0000000000001826.
Andersen, V, Fimland, MS, Mo, D-A, Iversen, VM, Vederhus, T, Rockland Hellebø, LR, Nordaune, KI, and Saeterbakken, AH. Electromyographic comparison of barbell deadlift, Hex bar deadlift, and hip thrust exercises: a cross-over study. J Strength Cond Res 32(3): 587-593, 2018-The aim of the study was to compare the muscle activation level of the gluteus maximus, biceps femoris, and erector spinae in the hip thrust, barbell deadlift, and Hex bar deadlift; each of which are compound resisted hip extension exercises. After 2 familiarization sessions, 13 resistance-trained men performed a 1 repetition maximum in all 3 exercises in 1 session, in randomized and counterbalanced order. The whole ascending movement (concentric phase), as well as its lower and upper parts (whole movement divided in 2), were analyzed. The hip thrust induced greater activation of the gluteus maximus compared with the Hex bar deadlift in the whole (16%, p = 0.025) and the upper part (26%, p = 0.015) of the movement. For the whole movement, the biceps femoris was more activated during barbell deadlift compared with both the Hex bar deadlift (28%, p < 0.001) and hip thrust (20%, p = 0.005). In the lower part of the movement, the biceps femoris activation was, respectively, 48% and 26% higher for the barbell deadlift (p < 0.001) and Hex bar deadlift (p = 0.049) compared with hip thrust. Biceps femoris activation in the upper part of the movement was 39% higher for the barbell deadlift compared with the Hex bar deadlift (p = 0.001) and 34% higher for the hip thrust compared with the Hex bar deadlift (p = 0.002). No differences were displayed for the erector spinae activation (p = 0.312-0.859). In conclusion, the barbell deadlift was clearly superior in activating the biceps femoris compared with the Hex bar deadlift and hip thrust, whereas the hip thrust provided the highest gluteus maximus activation.
Prenatal Diagnosis of Tay-Sachs Disease
Methods Mol Biol 2019;1885:233-250.PMID:30506202DOI:10.1007/978-1-4939-8889-1_16.
Tay-Sachs disease (TSD) is an autosomal recessive lysosomal storage disorder caused by mutations of the HEXA gene resulting in the deficiency of hexosaminidase A (Hex A) and subsequent neuronal accumulation of GM2 gangliosides. Infantile TSD is a devastating and fetal neurodegenerative disease with death before the age of 3-5 years. A small proportion of TSD patients carry milder mutations and may present juvenile or adult onset milder disease. TSD is more prevalent among Ashkenazi Jewish (AJ) individuals and some other genetically isolated populations with carrier frequencies of approximately ~1:27 which is much higher than that of 1:300 in the general population. Carrier screening and prenatal testing for TSD are effective in preventing the birth of affected fetuses greatly diminishing the incidence of TSD. Testing of targeted HEXA mutations by genotyping or sequencing can detect 98% of carriers in AJ individuals; however, the detection rate is much lower for most other ethnic groups. When combined with enzyme analysis, above 98% of carriers can be reliably identified regardless of ethnic background. Multiplex PCR followed by allele-specific primer extension is one method to test for known and common mutations. Sanger sequencing or other sequencing methods are useful to identify private mutations. For prenatal testing, only predefined parental mutations need to be tested. In the event of unknown mutational status or the presence of variants of unknown significance (VUS), enzyme analysis must be performed in conjunction with DNA-based assays to enhance the diagnostic accuracy. Enzymatic assays involve the use of synthetic substrates 4-methylumbelliferyl-N-acetyl-β-glucosamine (4-MUG) and 4-methylumbelliferyl-6-sulfo-2-acetamido-2-deoxy-β-D-glucopyranoside (4-MUGS) to measure the percentage Hex A activity (Hex A%) and specific Hex A activity respectively. These biochemical and molecular tests can be performed in both direct specimens and cultured cells from chorionic villi sampling or amniocentesis.
Hexarelin Protects Rodent Pancreatic Β-Cells Function from Cytotoxic Effects of Streptozotocin Involving Mitochondrial Signalling Pathways In Vivo and In Vitro
PLoS One 2016 Feb 26;11(2):e0149730.PMID:26918825DOI:10.1371/journal.pone.0149730.
Mitochondrial functions are crucial for pancreatic β-cell survival and glucose-induced insulin secretion. Hexarelin (Hex) is a synthetic small peptide ghrelin analogue, which has been shown to protect cardiomyocytes from the ischemia-reperfusion process. In this study, we used in vitro and in vivo models of streptozotocin (STZ)-induced β-cell damage to study the protective effect of Hex and the associated mechanisms. We found that STZ produced a cytotoxic effect in a dose- and time-dependent manner in MIN6 cells (a mouse β-cell line). Hex (1.0 μM) decreased the STZ-induced damage in β-cells. Rhodamine 123 assay and superoxide DHE production assay revealed that Hex ameliorated STZ-induced mitochondrial damage and excessive superoxide activity in β-cells. In addition, Hex significantly reduced STZ-induced expression of cleaved Caspases-3, Caspases-9 and the ratio of pro-apoptotic protein Bax to anti-apoptotic protein Bcl-2 in MIN6 cells. We further examined the in vivo effect of Hex in a rat model of type 1 diabetes induced by STZ injection. Hex ameliorated STZ-induced decrease in plasma insulin and protected the structure of islets from STZ-induced disruption. Hex also ameliorated STZ-induced expression of cleaved Caspase-9 and the Bax in β-cells. In conclusion, our data indicate that Hex is able to protects β-cell mass from STZ-caused cytotoxic effects involving mitochondrial pathways in vitro and in vivo. Hex may serve as a potential protective agent for the management of diabetes.
Homeoprotein Hex is expressed in mouse developing chondrocytes
J Biochem 2011 Jul;150(1):61-71.PMID:21454303DOI:10.1093/jb/mvr039.
Endochondral ossification is a complex process involving the formation of cartilage and the subsequent replacement by mineralized bone. Although the proliferation and differentiation of chondrocytes are strictly regulated, the molecular mechanisms involved are not completely understood. Here, we show that a divergent-type homeobox gene, hematopoietically expressed homeobox gene (Hex), is expressed in mouse chondrogenic cell line ATDC5. The expression of Hex protein drastically increased during differentiation. The chondrogenic differentiation-enhanced expression of Hex protein was also observed in chondrocytes in the tibia of embryonic day 15.5 (E15.5) mouse embryos. The localization of Hex protein in the chondrocytes of the tibia changed in association with maturation; namely, there was Hex protein in the cytoplasm near the endoplasmic reticulum (ER) in resting chondrocytes, which moved to the nucleus in prehypertrophic chondrocytes, and thereafter entered the ER in hypertrophic chondrocytes. These results suggest Hex expression and subcellular localization are associated with chondrocyte maturation.
Hex expression and localization in normal mammary gland and breast carcinoma
BMC Cancer 2006 Jul 19;6:192.PMID:16854221DOI:10.1186/1471-2407-6-192.
Background: The homeobox gene Hex is expressed in several cell types during different phases of animal development. It encodes for a protein localized in both the nucleus and the cytoplasm. During early mouse development, Hex is expressed in the primitive endoderm of blastocyst. Later, Hex is expressed in developing thyroid, liver, lung, as well as in haematopoietic progenitors and endothelial cells. Absence of nuclear expression has been observed during neoplastic transformation of the thyroid follicular cells. Aim of the present study was to evaluate the localization and the function of the protein Hex in normal and tumoral breast tissues and in breast cancer cell lines. Methods: Hex expression and nuclear localization were investigated by immunohistochemistry in normal and cancerous breast tissue, as well as in breast cancer cell lines. Hex mRNA levels were evaluated by real-time PCR. Effects of Hex expression on Sodium Iodide Symporter (NIS) gene promoter activity was investigated by HeLa cell transfection. Results: In normal breast Hex was detected both in the nucleus and in the cytoplasm. In both ductal and lobular breast carcinomas, a great reduction of nuclear Hex was observed. In several cells from normal breast tissue as well as in MCF-7 and T47D cell line, Hex was observed in the nucleolus. MCF-7 treatment with all-trans retinoic acid enhanced Hex expression and induced a diffuse nuclear localization. Enhanced Hex expression and diffuse nuclear localization were also obtained when MCF-7 cells were treated with inhibitors of histone deacetylases such as sodium butyrate and trichostatin A. With respect to normal non-lactating breast, the amount of nuclear Hex was greatly increased in lactating tissue. Transfection experiments demonstrated that Hex is able to up-regulate the activity of NIS promoter. Conclusion: Our data indicate that localization of Hex is regulated in epithelial breast cells. Since modification of localization occurs during lactation and tumorigenesis, we suggest that Hex may play a role in differentiation of the epithelial breast cell.