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C57BL/6JCya-Ndst1em1flox/Cya
Common Name:
Ndst1-flox
Product ID:
S-CKO-02998
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
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Basic Information
Strain Name
Ndst1-flox
Strain ID
CKOCMP-15531-Ndst1-B6J-VA
Gene Name
Ndst1
Product ID
S-CKO-02998
Gene Alias
1200015G06Rik; HSNST; HSNST 1; Hsst; N-HSST; N-HSST 1; NDST-1; b2b2230Clo
Background
C57BL/6JCya
NCBI ID
15531
Modification
Conditional knockout
Chromosome
18
Phenotype
MGI:104719
Document
Click here to download >>
Application
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Rare Disease Data Center >>
Note
Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Ndst1em1flox/Cya mice (Catalog S-CKO-02998) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000169273
NCBI RefSeq
NM_001348101
Target Region
Exon 3
Size of Effective Region
~1.2 kb
Detailed Document
Click here to download >>
Overview of Gene Research
Ndst1, also known as N-deacetylase / N-sulfotransferase, is a key enzyme in heparan sulfate (HS) biosynthesis, responsible for N-deacetylation and N-sulfation of N-acetyl-glucosamine residues. This step influences downstream enzymatic modifications, determining the overall structure and sulfation degree of the HS polysaccharide chain. HS is an important extracellular matrix component involved in various signaling pathways, such as Wnt, BMP, and prion-related processes, thus making Ndst1 crucial for normal development and physiological functions [4,7,8]. Genetic models, like knockout (KO) and conditional knockout (CKO) mice, are valuable tools for studying Ndst1 functions.

In conditional knockout mouse studies, neuronal Ndst1-depleted mice infected with extracellular, plaque-forming prions survived longer, showing fewer and smaller parenchymal plaques, shorter fibrils, and increased vascular amyloid, suggesting enhanced aggregate clearance. This indicates that HS sulfate groups (regulated by Ndst1) hinder the transit of extracellular prion protein monomers [1]. In Xenopus embryos, ndst1 overexpression expanded the neural crest region, while translational inhibition reduced the trigeminal and adjacent neural crest regions, and ndst1-knocked-down embryos showed cranial ganglion formation defects. Ndst1 was also found to activate the Wnt signaling pathway at the neurula stage [2]. In murine adipose-derived stem cells, overexpression of NDST1 suppressed osteogenic differentiation, induced chemokine production under TNF-α stimulation, and attenuated the fibrotic response [3]. In HPH-induced RVH rats, increased NDST1 was observed, and in vitro cell experiments showed that inhibiting NDST1 expression enhanced cell viability, reduced apoptosis, and alleviated cardiomyocyte hypertrophy [5]. In Ndst1(-/-) mice, defective lung cell differentiation, increased cell proliferation, and enhanced downstream BMP signaling were found, with exogenous heparin able to rescue BMP signaling and internalization abnormalities [6].

In conclusion, Ndst1 is essential for proper functioning in multiple biological processes including embryonic development, neural patterning, stem cell function, and disease-related pathways such as prion-associated neurodegeneration, hypoxic pulmonary hypertension-induced right ventricular hypertrophy, and fibrotic response. The use of Ndst1 KO/CKO mouse models has significantly contributed to understanding its role in these disease areas, providing insights into potential therapeutic targets.

References:
1. Aguilar-Calvo, Patricia, Malik, Adela, Sandoval, Daniel R, Esko, Jeffrey D, Sigurdson, Christina J. 2023. Neuronal Ndst1 depletion accelerates prion protein clearance and slows neurodegeneration in prion infection. In PLoS pathogens, 19, e1011487. doi:10.1371/journal.ppat.1011487. https://pubmed.ncbi.nlm.nih.gov/37747931/
2. Yamamoto, Takayoshi, Kambayashi, Yuta, Tsukano, Kohei, Michiue, Tatsuo. 2023. Ndst1, a heparan sulfate modification enzyme, regulates neuroectodermal patterning by enhancing Wnt signaling in Xenopus. In Development, growth & differentiation, 65, 153-160. doi:10.1111/dgd.12843. https://pubmed.ncbi.nlm.nih.gov/36726238/
3. Otsuka, Takayoshi, Kan, Ho-Man, Mason, Timothy D, Nair, Lakshmi S, Laurencin, Cato T. 2022. Overexpression of NDST1 Attenuates Fibrotic Response in Murine Adipose-Derived Stem Cells. In Stem cells and development, 31, 787-798. doi:10.1089/scd.2022.0053. https://pubmed.ncbi.nlm.nih.gov/35920108/
4. Reuter, Miriam S, Musante, Luciana, Hu, Hao, Reis, André, Kahrizi, Kimia. 2014. NDST1 missense mutations in autosomal recessive intellectual disability. In American journal of medical genetics. Part A, 164A, 2753-63. doi:10.1002/ajmg.a.36723. https://pubmed.ncbi.nlm.nih.gov/25125150/
5. Sun, Haixia, Liu, Junling, Su, Yuxin, Li, Jia, Song, Meiling. . The role and mechanism of NDST1/NULP1 regulating right ventricular hypertrophy in hypoxic pulmonary hypertension. In General physiology and biophysics, 41, 407-416. doi:10.4149/gpb_2022032. https://pubmed.ncbi.nlm.nih.gov/36222339/
6. Hu, Zhonghua, Wang, Chaochen, Xiao, Ying, Jing, Naihe, Hu, Gengxi. 2009. NDST1-dependent heparan sulfate regulates BMP signaling and internalization in lung development. In Journal of cell science, 122, 1145-54. doi:10.1242/jcs.034736. https://pubmed.ncbi.nlm.nih.gov/19299468/
7. Khosrowabadi, Elham, Mignon-Ravix, Cécile, Riccardi, Florence, Kjellén, Lena, Molinari, Florence. . Loss of NDST1 N-sulfotransferase activity is associated with autosomal recessive intellectual disability. In Human molecular genetics, 33, 520-529. doi:10.1093/hmg/ddad203. https://pubmed.ncbi.nlm.nih.gov/38129107/
8. Missaghian, Parisa, Dierker, Tabea, Khosrowabadi, Elham, Kellokumpu, Sakari, Kjellén, Lena. . A dominant negative splice variant of the heparan sulfate biosynthesis enzyme NDST1 reduces heparan sulfate sulfation. In Glycobiology, 32, 518-528. doi:10.1093/glycob/cwac004. https://pubmed.ncbi.nlm.nih.gov/35137078/
Quality Control Standard
Sperm Test

Pre-cryopreservation: Measurement of sperm concentration, determination of sperm viability.

Post-cryopreservation: A vial of cryopreserved sperms is selected for in-vitro fertilization from each batch.

Environmental Standards:SPF
Available Region:Global
Source:Cyagen
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