Anti-CHST3 polyclonal antibody (DPAB-DC3831)

Mouse anti-Human CHST3 (aa 312-411) polyclonal antibody for WB, ELISA

Specifications


Host Species
Mouse
Species Reactivity
Human
Immunogen
CHST3 (NP_004264, 312 a.a. ~ 411 a.a) partial recombinant protein with GST tag. The sequence is VAFAGKYKTWKKWLDDEGQDGLREEEVQRLRGNCESIRLSAELGLRQPAWLRGRYMLVRYEDVARGPLQKAREMYRFAGIPLTPQVEDWIQKNTQAAHDG
Conjugate
Unconjugated

Target


Alternative Names
CHST3; carbohydrate (chondroitin 6) sulfotransferase 3; HSD; C6ST; C6ST1; carbohydrate sulfotransferase 3
Entrez Gene ID
UniProt ID

Product Background


Gene summary
CHST3 (Carbohydrate (Chondroitin 6) Sulfotransferase 3) is a Protein Coding gene. Diseases associated with CHST3 include spondyloepiphyseal dysplasia with congenital joint dislocations and larsen syndrome, autosomal recessive. Among its related pathways are Metabolism and Glycosaminoglycan metabolism. GO annotations related to this gene include sulfotransferase activity and chondroitin 6-sulfotransferase activity. An important paralog of this gene is CHST2. This gene encodes an enzyme which catalyzes the sulfation of chondroitin, a proteoglycan found in the extracellular matrix and most cells which is involved in cell migration and differentiation. Mutations in this gene are associated with spondylepiphyseal dysplasia and humerospinal dysostosis.
Antigen Description
This gene encodes an enzyme which catalyzes the sulfation of chondroitin, a proteoglycan found in the extracellular matrix and most cells which is involved in cell migration and differentiation. Mutations in this gene are associated with spondylepiphyseal dysplasia and humerospinal dysostosis. Spondyloepiphyseal dysplasia with congenital joint dislocations (SEDC-JD) [MIM:143095]: A bone dysplasia clinically characterized by dislocation of the knees and/or hips at birth, clubfoot, elbow joint dysplasia with subluxation and limited extension, short stature, and progressive kyphosis developing in late childhood. The disorder is usually evident at birth, with short stature and multiple joint dislocations or subluxations that dominate the neonatal clinical and radiographic picture. During childhood, the dislocations improve, both spontaneously and with surgical treatment, and features of spondyloepiphyseal dysplasia become apparent, leading to arthritis of the hips and spine with intervertebral disk degeneration, rigid kyphoscoliosis, and trunk shortening by late childhood. Note=The disease is caused by mutations affecting the gene represented in this entry. The function about CHST3 antigen include chondroitin 6-sulfotransferase activity; proteoglycan sulfotransferase activity; sulfotransferase activity.
Pathway
Chondroitin sulfate biosynthesis; Disease; Glycosaminoglycan biosynthesis - chondroitin sulfate / dermatan sulfate; Glycosaminoglycan metabolism.

Citations


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References


Differential Use of Chondroitin Sulfate to Regulate Hyaluronan Binding by Receptor CD44 in Inflammatory and Interleukin 4-activated Macrophages

JOURNAL OF BIOLOGICAL CHEMISTRY

Authors: Ruffell, Brian; Poon, Grace F. T.; Lee, Sally S. M.; Brown, Kelly L.; Tjew, Sie-Lung; Cooper, Jessie; Johnson, Pauline

CD44 is a cell surface receptor for the extracellular matrix glycosaminoglycan hyaluronan and is involved in processes ranging from leukocyte recruitment to wound healing. In the immune system, the binding of hyaluronan to CD44 is tightly regulated, and exposure of human peripheral blood monocytes to inflammatory stimuli increases CD44 expression and induces hyaluronan binding. Here we sought to understand how mouse macrophages regulate hyaluronan binding upon inflammatory and anti-inflammatory stimuli. Mouse bone marrow-derived macrophages stimulated with tumor necrosis factor alpha or lipopolysaccharide and interferon-gamma (LPS/IFN gamma) induced hyaluronan binding by up-regulating CD44 and down-regulating chondroitin sulfation on CD44. Hyaluronan binding was induced to a lesser extent in interleukin-4 (IL-4)-activated macrophages despite increased CD44 expression, and this was attributable to increased chondroitin sulfation on CD44, as treatment with beta-D-xyloside to prevent chondroitin sulfate addition significantly enhanced hyaluronan binding. These changes in the chondroitin sulfation of CD44 were associated with changes in mRNA expression of two chondroitin sulfotransferases, CHST3 and CHST7, which were decreased in LPS/IFN gamma-stimulated macrophages and increased in IL-4-stimulated macrophages. Thus, inflammatory and anti-inflammatory stimuli differentially regulate the chondroitin sulfation of CD44, which is a dynamic physiological regulator of hyaluronan binding by CD44 in mouse macrophages.

Lysophosphatidic acid receptor 5 transactivation of TGFBR1 stimulates the mRNA expression of proteoglycan synthesizing genes XYLT1 and CHST3

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH

Authors: Zhou, Ying; Little, Peter J.; Cao, Yingnan; Ta, Hang T.; Kamato, Danielle

Lysophosphatidic acid (LPA) via transactivation dependent signalling pathways contributes to a plethora of physiological and pathophysiological responses. In the vasculature, hyperelongation of glycosaminoglycan (GAG) chains on proteoglycans leads to lipid retention in the intima resulting in the early pathogenesis of atherosclerosis. Therefore, we investigated and defined the contribution of transactivation dependent signalling in LPA mediated GAG chain hyperelongation in human vascular smooth muscle cells (VSMCs). LPA acting via the LPA receptor 5 (LPAR5) transactivates the TGFBR1 to stimulate the mRNA expression of GAG initiation and elongation genes xylosyltransferase-1 (XYLT1) and chondroitin 6-sulfotransferase-1 (CHST3), respectively. We found that LPA stimulates ROS and Akt signalling in VSMCs, however they are not associated in LPAR5 transactivation of the TGFBR1. We observed that LPA via ROCK dependent pathways transactivates the TGFBR1 to stimulate genes associated with GAG chain elongation. We demonstrate that GPCR transactivation of the TGFBR1 occurs via a universal biochemical mechanism and the identified effectors represent potential therapeutic targets to inhibit pathophysiological effects of GPCR transactivation of the TGFBR1.

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