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Search results for: WISP2

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#38717632   2024/05/08 To Up

Oxidative DNA damage promotes vascular aging associated with changes in extracellular matrix-regulating proteins.

Vascular aging is characterized by vessel stiffening, with increased deposition of extracellular matrix (ECM) proteins including collagens. Oxidative DNA damage occurs in vascular aging, but how it regulates ECM proteins and vascular stiffening is unknown. We sought to determine the relationship between oxidative DNA damage and ECM regulatory proteins in vascular aging.
Kirsty Foote, Marieke Rienks, Lukas Schmidt, Konstantinos Theofilatos, Yasmin, Matiss Ozols, Alexander Eckersley, Aarti Shah, Nichola Figg, Alison Finigan, Kevin O'Shaughnessy, Ian B Wilkinson, Manuel Mayr, Martin Bennett

1130 related Products with: Oxidative DNA damage promotes vascular aging associated with changes in extracellular matrix-regulating proteins.

2 Pieces/Box1 ml50 505010001mg100 5096 tests101 mg

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#38177997   2024/01/04 To Up

Analysis of the differentially expressed genes in the combs and testes of Qingyuan partridge roosters at different developmental stages.

The sexual maturity of chickens is an important economic trait, and the breeding of precocious and delayed puberty roosters is an important selection strategy for broilers. The comb serves as an important secondary sexual characteristic of roosters and determines their sexual precocity. Moreover, comb development is closely associated with gonad development in roosters. However, the underlying molecular mechanism regulating the sexual maturity of roosters has not yet been fully explored.
Hao Qi, Zhidan Deng, Fei Ye, Junwei Gou, Miaoxin Huang, Hai Xiang, Hua Li

2567 related Products with: Analysis of the differentially expressed genes in the combs and testes of Qingyuan partridge roosters at different developmental stages.

11500IU

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#38035707   // To Up

SNHG3/WISP2 Axis Promotes Hela Cell Migration and Invasion Activating Wnt/β-Catenin Signaling.

Cervical cancer (CC) poses a significant threat to women's health and has a relatively poor prognosis due to local invasion and metastasis. It is, therefore, crucial to elucidate the molecular mechanisms of CC metastasis. SNHG3 has been implicated in various tumor metastasis processes, but its involvement in CC has not been thoroughly studied. Our study aimed to investigate the role of SNHG3 in metastasis and elucidate its underlying mechanisms in CC.
Dengfei Xu, Hao Feng, Zirui Ren, Xiang Li, Chenyang Jiang, Yuming Chen, Lina Liu, Wenchao Chen, Zhilei Cui, Shundong Cang

2807 related Products with: SNHG3/WISP2 Axis Promotes Hela Cell Migration and Invasion Activating Wnt/β-Catenin Signaling.

24 tests96 samples50ug424 tests100 ug24 tests50ug96 samples100 ug1.5 x 10^6 cells500ug

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#37794318   2023/10/04 To Up

A positive association of serum CCN5/WISP2 levels with the risk of developing gestational diabetes mellitus: a case-control study.

CCN5/WISP2 is prominently manifest in adipose tissue and has been linked to the pathogenesis of obesity, diabetes, and insulin resistance. However, discrepancies exist in previous studies, and little is known about its association with gestational diabetes mellitus (GDM). The current investigation is designed to examine the correlation of WISP2 with risk factors in GDM patients in comparison to healthy pregnant women for the first time.
Mohammed Farhan Hamdan Alshganbee, Fariba Nabatchian, Vida Farrokhi, Reza Fadaei, Nariman Moradi, Reza Afrisham

2634 related Products with: A positive association of serum CCN5/WISP2 levels with the risk of developing gestational diabetes mellitus: a case-control study.

10.00 nmol1. Set25.00 nmol100 ml5.00 nmol5 g100ug200ul96T

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#37554458   2023/07/13 To Up

Magneto-mechanical stimulation modulates osteocyte fate via the ECM-integrin-CSK axis and wnt pathway.

Osteocytes are the mechano-sensors of bones. Large gradient high-static magnetic fields (LG-HMFs) produce stable, high-precision, and non-attenuation mechanical forces. We discovered that magnetic forces opposite to gravity inhibited MLO-Y4 osteocyte proliferation and viability by inducing structural damage and apoptosis. In contrast, magnetic force loading in the same direction as that of gravity promoted the proliferation and inhibited apoptosis of MLO-Y4 osteocytes. Differentially expressed gene (DEG) analysis after magnetic force stimulation indicated that the ECM-integrin-CSK axis responded most significantly to mechanical signals. was the most significant DEG between the 12 T upward and downward groups, showing the highest correlation with the Wnt pathway according to the STRING protein interaction database. Explaining the cellular and molecular mechanisms by which mechanical stimuli influence bone remodeling is currently the focus of osteocyte-related research. Our findings provide insights into the effects of LG-HMFs on bone cells, which have further implications in clinical practice.
Bin Zhang, Xianglin Li, Xiaojie Zhou, ChenGe Lou, Shenghang Wang, Huanhuan Lv, Gejing Zhang, Yanwen Fang, Dachuan Yin, Peng Shang

1664 related Products with: Magneto-mechanical stimulation modulates osteocyte fate via the ECM-integrin-CSK axis and wnt pathway.

100ug Lyophilized1.00 mg100ug/vial50 ug100ug Lyophilized25 mg100ug500 Units100 per bag, 10 bags per100ug Lyophilized3 Modulators100 ug/vial

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#37302424   2023/06/09 To Up

WISP2 downregulation inhibits the osteogenic differentiation of BMSCs in congenital scoliosis by regulating Wnt/β-catenin pathway.

Bone marrow mesenchymal stem cells (BMSCs) are instrumental in bone development, metabolism, and marrow microenvironment homeostasis. Despite this, the relevant effects and mechanisms of BMSCs on congenital scoliosis (CS) remain undefined. Herein, it becomes our focus to reveal the corresponding effects and mechanisms implicated.
Yang Zheng, Panyang Shen, Mengsha Tong, Hangchao Li, Conglin Ren, Fengqing Wu, Hanyu Li, Huan Yang, Bingbing Cai, Weibin Du, Xing Zhao, Shasha Yao, Renfu Quan

1907 related Products with: WISP2 downregulation inhibits the osteogenic differentiation of BMSCs in congenital scoliosis by regulating Wnt/β-catenin pathway.

2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box100 μg2 Pieces/Box2 Pieces/Box1

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#37195381   2023/05/17 To Up

CCN proteins: opportunities for clinical studies-a personal perspective.

The diverse members of the CCN family now designated as CCN1(CYR61), CCN2 (CTGF), CCN3(NOV), CCN4(WISP1), CCN5(WISP2), CCN6(WISP3) are a conserved matricellular family of proteins exhibiting a spectrum of functional properties throughout all organs in the body. Interaction with cell membrane receptors such as integrins trigger intracellular signaling pathways. Proteolytically cleaved fragments (constituting the active domains) can be transported to the nucleus and perform transcriptional relevant functional activities. Notably, as also found in other protein families some members act opposite to others creating a system of functionally relevant checks and balances. It has become apparent that these proteins are secreted into the circulation, are quantifiable, and can serve as disease biomarkers. How they might also serve as homeostatic regulators is just becoming appreciated. In this review I have attempted to highlight the most recent evidence under the subcategories of cancer and non-cancer relevant that could lead to potential therapeutic approaches or ideas that can be factored into clinical advances. I have added my own personal perspective on feasibility.
Herman Yeger

2639 related Products with: CCN proteins: opportunities for clinical studies-a personal perspective.

2 Pieces/Box100.1mg1 mg0.1 mg1mg1mg1mg100

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#37166689   2023/05/11 To Up

Expression and biological function of the cellular communication network factor 5 (CCN5) in primary liver cells.

The cellular (centralized) communication network (CCN) factor protein family contains six small secreted cysteine-rich proteins sharing high structural similarity. These matricellular proteins have vital biological functions in cell adhesion, migration, cell cycle progression, and control of production and degradation of extracellular matrix. However, in liver the biological functions of CCN proteins become most visible during hepatic injury, disease, and remodeling. In particular, most of the hepatic functions of CCN proteins were derived from CCN2/CTGF, which becomes highly expressed in damaged hepatocytes and acts as a profibrogenic molecule. On the contrary, CCN1/CYR61 seems to have opposite effects, while the biological activity during hepatic fibrosis is somewhat controversially discussed for other CCN family members. In the present study, we analyzed the expression of CCN5/WISP2 in cultures of different types of primary liver cells and in an experimental model of hepatic fibrosis. We found that CCN5 is expressed in hepatic stellate cells, myofibroblasts and portal myofibroblasts, while CCN5 expression is virtually absent in hepatocytes. During hepatic fibrogenesis, CCN5 is significantly upregulated. Overexpression of CCN5 in portal myofibroblasts reduced expression of transforming growth factor-β receptor I (ALK5) and concomitant Smad2 activation, whereas JunB expression is upregulated. Moreover, elevated expression of CCN5 induces endoplasmic reticulum stress, unfolded protein response and apoptosis in portal myofibroblasts. We suggest that upregulated expression of CCN5 might be an intrinsic control mechanism that counteracts overshooting fibrotic responses in profibrogenic liver cells.
Erawan Borkham-Kamphorst, Steffen K Meurer, Ralf Weiskirchen

2269 related Products with: Expression and biological function of the cellular communication network factor 5 (CCN5) in primary liver cells.

10 ug1 mg100.00 ug1.00 flask100 5 mg50 ug

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#36801505   2023/02/06 To Up

LncRNA TRG-AS1 inhibits bone metastasis of breast cancer by the miR-877-5p/WISP2 axis.

TRG-AS1 has been proved to inhibit cancer progression, whereas its effect on bone metastases of breast cancer is unknown. In this study, we determined breast cancer patients with disease free survival is longer in breast cancer patients with high TRG-AS1 expression. Moreover, TRG-AS1 was downregulated in breast cancer tissues and even lower in bone metastatic tumor tissues. Compared with parental breast cancer cell MDA-MB-231, TRG-AS1 expression was downregulated in MDA-MB-231-BO cells with strong bone-metastatic characteristics. Next, the binding sites of miR-877-5p on TRG-AS1 and WISP2 mRNA were predicted and result showed that miR-877-5p could bind to 3'UTR of TRG-AS1 and WISP2. Subsequently, BMMs and MC3T3-E1 cells were cultured in the conditioned media of MDA-MB-231 BO cells transfected with TRG-AS1 overexpression vector, shRNA and/or miR-877-5p mimics or inhibitor and/or overexpression vector and small interfering RNA of WISP2. TRG-AS1 silencing or miR-877-5p overexpression promoted MDA-MB-231 BO cell proliferation and invasion. TRG-AS1 overexpressing reduced TRAP positive cells, decreased TRAP, Cathepsin K, c-Fos, NFATc1 and AREG expression in BMMs, and promoted OPG, Runx2 and Bglap2 expression, and decreased RANKL expression in MC3T3-E1 cells. Silencing WISP2 rescued the effect of TRG-AS1 on BMMs and MC3T3-E1 cells. In vivo results showed that tumor volumes significantly decreased in mice injected with LV-TRG-AS1 transfected MDA-MB-231 cells. TRG-AS1 knockdown markedly reduced the number of TRAP+ cells and the percentage of Ki-67+ cells and decreased E-cadherin expression in xenograft tumor mice. In summary, TRG-AS1 acts an endogenous RNA, inhibited breast cancer bone metastasis by competitively binding with miR-877-5p to upregulate WISP2 expression.
Jinxiang Zhu, Hao Dai, Xiang Li, Longwei Guo, Xin Sun, Zhiwei Zheng, Chongwen Xu

1732 related Products with: LncRNA TRG-AS1 inhibits bone metastasis of breast cancer by the miR-877-5p/WISP2 axis.



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#36736423   2023/02/01 To Up

Acetylation stabilizes the signaling protein WISP2 by preventing its degradation to suppress the progression of acute myeloid leukemia.

Acute myeloid leukemia (AML) is challenging to treat due to its heterogeneity, prompting a deep understanding of its pathogenesis mechanisms, diagnosis, and treatment. Here, we found reduced expression and acetylation levels of WISP2 in bone marrow mononuclear cells from AML patients and that AML patients with lower WISP2 expression tended to have reduced survival. At the functional level, overexpression of WISP2 in leukemia cells (HL-60 and Kasumi-1) suppressed cell proliferation, induced cell apoptosis, and exerted antileukemic effects in an in vivo model of AML. Our mechanistic investigation demonstrated that WISP2 deacetylation was regulated by the deacetylase histone deacetylase (HDAC)3. In addition, we determined that crosstalk between acetylation and ubiquitination was involved in the modulation of WISP2 expression in AML. Deacetylation of WISP2 decreased the stability of the WISP2 protein by boosting its ubiquitination mediated by NEDD4 and proteasomal degradation. Moreover, pan-HDAC inhibitors (valproic acid and trichostatin A) and an HDAC3-specific inhibitor (RGFP966) induced WISP2 acetylation at lysine K6 and prevented WISP2 degradation. This regulation led to inhibition of proliferation and induction of apoptosis in AML cells. In summary, our study revealed that WISP2 contributes to tumor suppression in AML, which provided an experimental framework for WISP2 as a candidate for gene therapy of AML.
Hao Zhang, Wenjun Song, Xinying Ma, Mingxiao Yu, Lulu Chen, Yanling Tao

1569 related Products with: Acetylation stabilizes the signaling protein WISP2 by preventing its degradation to suppress the progression of acute myeloid leukemia.

100 U1mg1021500IU 100ul

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