InVivoMAb anti-mouse CD29
in vitro CD29 neutralization
Immunofluorescence
Flow cytometry
Product Description
Specifications
| Isotype | Rat IgG2a, κ |
|---|---|
| Recommended Isotype Control(s) | InVivoMAb rat IgG2a isotype control, anti-trinitrophenol |
| Recommended Dilution Buffer | InVivoPure pH 7.0 Dilution Buffer |
| Conjugation | This product is unconjugated. Conjugation is available via our Antibody Conjugation Services. |
| Immunogen | C57BL/6 x DBA/2 mouse bone-marrow stromal cell clone BMS2 |
| Reported Applications |
in vivo CD29 neutralization in vitro CD29 neutralization Immunofluorescence Flow cytometry |
| Formulation |
PBS, pH 7.0 Contains no stabilizers or preservatives |
| Endotoxin |
≤1EU/mg (≤0.001EU/μg) Determined by LAL assay |
| Purity |
≥95% Determined by SDS-PAGE |
| Sterility | 0.2 µm filtration |
| Production | Purified from cell culture supernatant in an animal-free facility |
| Purification | Protein G |
| RRID | AB_2687714 |
| Molecular Weight | 150 kDa |
| Storage | The antibody solution should be stored at the stock concentration at 4°C. Do not freeze. |
| Need a Custom Formulation? | See All Antibody Customization Options |
Application References
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Bayik, D., et al (2021). "Distinct cell adhesion signature defines glioblastoma myeloid-derived suppressor cell subsets" bioRxiv : 2021.2009.2027.461995.
Increased myeloid-derived suppressor cell (MDSC) frequency is associated with worse outcomes and poor therapeutic response in glioblastoma (GBM). Monocytic (m) MDSCs represent the predominant subset in the GBM microenvironment. However, the molecular basis of mMDSC enrichment in the tumor microenvironment compared to granulocytic (g) MDSCs has yet to be determined. Here, we report that mMDSCs and gMDSCs display differences in their tumoraccelerating ability, with mMDSCs driving tumor growth in GBM models. Epigenetic assessments indicate enhanced gene accessibility for cell adhesion programs in mMDSCs and higher cellsurface integrin expression in mouse and human mMDSCs. Integrin β1 blockage abrogated the tumor-promoting phenotype of mMDSCs and altered the immune profile in the tumor microenvironment. These findings suggest that integrin β1 expression underlies the enrichment of mMDSCs in tumors and represents a putative immunotherapy target to attenuate myeloid cell-driven immune suppression in GBM.Summary Myeloid-derived suppressor cells (MDSCs) drive glioblastoma growth; however, the function of specific MDSCs subsets is unclear. Bayik et al. demonstrate that adhesion programs are enhanced in monocytic MDSCs and responsible for their GBM-promoting function.Competing Interest StatementY. Fan is a co-founder of Radix Therapeutics. All other authors declare no competing interests.
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Manieri, N. A., et al (2015). "Mucosally transplanted mesenchymal stem cells stimulate intestinal healing by promoting angiogenesis" J Clin Invest 125(9): 3606-3618.
PubMed
Mesenchymal stem cell (MSC) therapy is an emerging field of regenerative medicine; however, it is often unclear how these cells mediate repair. Here, we investigated the use of MSCs in the treatment of intestinal disease and modeled abnormal repair by creating focal wounds in the colonic mucosa of prostaglandin-deficient mice. These wounds developed into ulcers that infiltrated the outer intestinal wall. We determined that penetrating ulcer formation in this model resulted from increased hypoxia and smooth muscle wall necrosis. Prostaglandin I2 (PGI2) stimulated VEGF-dependent angiogenesis to prevent penetrating ulcers. Treatment of mucosally injured WT mice with a VEGFR inhibitor resulted in the development of penetrating ulcers, further demonstrating that VEGF is critical for mucosal repair. We next used this model to address the role of transplanted colonic MSCs (cMSCs) in intestinal repair. Compared with intravenously injected cMSCs, mucosally injected cMSCs more effectively prevented the development of penetrating ulcers, as they were more efficiently recruited to colonic wounds. Importantly, mucosally injected cMSCs stimulated angiogenesis in a VEGF-dependent manner. Together, our results reveal that penetrating ulcer formation results from a reduction of local angiogenesis and targeted injection of MSCs can optimize transplantation therapy. Moreover, local MSC injection has potential for treating diseases with features of abnormal angiogenesis and repair.
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Pinho, S., et al (2013). "PDGFRalpha and CD51 mark human nestin+ sphere-forming mesenchymal stem cells capable of hematopoietic progenitor cell expansion" J Exp Med 210(7): 1351-1367.
PubMed
The intermediate filament protein Nestin labels populations of stem/progenitor cells, including self-renewing mesenchymal stem cells (MSCs), a major constituent of the hematopoietic stem cell (HSC) niche. However, the intracellular location of Nestin prevents its use for prospective live cell isolation. Hence it is important to find surface markers specific for Nestin(+) cells. In this study, we show that the expression of PDGFRalpha and CD51 among CD45(-) Ter119(-) CD31(-) mouse bone marrow (BM) stromal cells characterizes a large fraction of Nestin(+) cells, containing most fibroblastic CFUs, mesenspheres, and self-renewal capacity after transplantation. The PDGFRalpha(+) CD51 (+)subset of Nestin(+) cells is also enriched in major HSC maintenance genes, supporting the notion that niche activity co-segregates with MSC activity. Furthermore, we show that PDGFRalpha(+) CD51(+) cells in the human fetal BM represent a small subset of CD146(+) cells expressing Nestin and enriched for MSC and HSC niche activities. Importantly, cultured human PDGFRalpha(+) CD51(+) nonadherent mesenspheres can significantly expand multipotent hematopoietic progenitors able to engraft immunodeficient mice. These results thus indicate that the HSC niche is conserved between the murine and human species and suggest that highly purified nonadherent cultures of niche cells may represent a useful novel technology to culture human hematopoietic stem and progenitor cells.
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Manieri, N. A., et al (2012). "Igf2bp1 is required for full induction of Ptgs2 mRNA in colonic mesenchymal stem cells in mice" Gastroenterology 143(1): 110-121 e110.
PubMed
BACKGROUND & AIMS: Prostaglandin-endoperoxide synthase (Ptgs)2 is an enzyme involved in prostaglandin production during the response to mucosal damage. Its expression is regulated, in part, by messenger RNA (mRNA)-binding proteins that control the stability of Ptgs2 mRNA. We used a precise system of colonic injury and repair to identify Ptgs2 mRNA-binding proteins. METHODS: We used endoscopy-guided mucosal excision to create focal injury sites in colons of mice. Wound beds from wild-type, Ptgs2(-/-), Ptgs2(+/-), and Myd88(-/-) mice were analyzed at 2-day intervals after injury for aspects of repair and Ptgs2 expression. We used cultured colonic mesenchymal stem cells (cMSCs) that express Ptgs2 to identify and analyze molecules that regulate Ptgs2 expression. RESULTS: Ptgs2(-/-) mice had defects in wound repair, validating the biopsy technique as a system to study the regulation of Ptgs2. Ptgs2(+/-) mice had similar defects in wound healing, so full induction of Ptgs2 is required for wound repair. In wild-type mice, levels of Ptgs2 mRNA increased significantly in the wound bed 2 and 4 days after injury; the highest levels of Ptgs2 were observed in cMSCs. In a functional short hairpin RNA knockdown screen, we identified Igf2bp1, a VICKZ (Vg1 RNA binding protein, Insulin-like growth factor II mRNA binding protein 1, Coding region determinant-binding protein, KH domain containing protein overexpressed in cancer, and Zipcode-binding protein-1) mRNA-binding protein, as a regulator of Ptgs2 expression in cMSCs. Igf2bp1 also interacted physically with Ptgs2 mRNA. Igf2bp1 expression was induced exclusively in wound-bed cMSCs, and full induction of Ptgs2 and Igf2bp1 during repair required Myd88. CONCLUSIONS: We identified Igf2bp1 as a regulator of Ptgs2 mRNA in mice. Igf2bp1 is required for full induction of Ptgs2 mRNA in cMSCs.
Product Citations
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Immune Niche Formation Reveals Mechanisms of Tumor Dormancy and Targeting Opportunities
In Research Square on 2 February 2026 by Yang, L., Ahad, A., et al.
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Semaphorin 7A Regulates the Balance Between Cartilaginous and Fibrous Tissues in the Repair Process of Articular Cartilage Damage.
In Cartilage on 31 January 2026 by Hatada, R., Abe, K., et al.
PubMed
ObjectiveDamage to the joint-surface repair itself as fibrocartilage, a mixture of cartilaginous and fibrous tissues, which leads to debilitating conditions with persistent joint pain. The regulatory mechanisms that control the formation of these tissues are poorly understood.MethodsWe analyzed single-cell RNA-sequencing data from the repaired tissue formed in a chondral defect model of the monkey knee joint to identify genes specifically expressed in the repaired tissue. We used primary chondrocytes from semaphorin 7A (Sema7A) knockout mice to analyze the function of Sema7A in the dedifferentiation of chondrocytes in vitro. We introduced articular cartilage defect model in the knee joints in Sema7A knockout mice.ResultsSingle-cell RNA-sequencing analysis revealed that Sema7A is specifically expressed in the cartilaginous tissue in the repaired tissue formed in the articular cartilage defect. In vitro analysis showed that Sema7A autonomously induced the dedifferentiation of chondrocytes at passage 2, which is assumed to correspond to cartilaginous tissue cells, toward a fibroblastic state. In addition, Sema7A heteronomously suppressed the re-differentiation of passage 8 fibroblastic cells, which were assumed to correspond to fibrous tissue cells. Addition of anti-integrin β1 neutralizing antibody abolished Sema7A-induced suppression of Col2a1 and Col9a1 expression, suggesting that integrin β1 mediates Sema7A function. Sema7A knockout mice showed significantly improved healing in an articular surface defect model of the knee joints. Sema7A deletion increased cartilaginous tissue formation and decreased fibrous tissue formation in joint-surface defects.ConclusionsSema7A regulates the balance between cartilaginous and fibrous tissues during articular cartilage damage repair.
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Integrin-mediated mTOR signaling drives TGF-β overactivity and myxomatous mitral valve degeneration in hypomorphic fibrillin-1 mice.
In J Clin Invest on 15 July 2025 by Gao, F., Chen, Q., et al.
PubMed
Mitral valve prolapse is often benign, but progression to mitral regurgitation may require invasive intervention and there is no specific medical therapy. An association of mitral valve prolapse with Marfan syndrome resulting from pathogenic FBN1 variants supports the use of hypomorphic fibrillin-1 mgR mice to investigate mechanisms and therapy for mitral valve disease. mgR mice developed severe myxomatous mitral valve degeneration with mitral regurgitation by 12 weeks of age. Persistent activation of TGF-β and mTOR signaling along with macrophage recruitment preceded histological changes at 4 weeks of age. Short-term mTOR inhibition with rapamycin from 4 to 5 weeks of age prevented TGF-β overactivity and leukocytic infiltrates, while long-term inhibition of mTOR or TGF-β signaling from 4 to 12 weeks of age rescued mitral valve leaflet degeneration. Transcriptomic analysis identified integrins as key receptors in signaling interactions, and serologic neutralization of integrin signaling or a chimeric integrin receptor altering signaling prevented mTOR activation. We confirmed increased mTOR signaling and a conserved transcriptome signature in human specimens of sporadic mitral valve prolapse. Thus, mTOR activation from abnormal integrin-dependent cell-matrix interactions drives TGF-β overactivity and myxomatous mitral valve degeneration, and mTOR inhibition may prevent disease progression of mitral valve prolapse.
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Distinct Cell Adhesion Signature Defines Glioblastoma Myeloid-Derived Suppressor Cell Subsets.
In Cancer Res on 15 November 2022 by Bayik, D., Bartels, C. F., et al.
PubMed
In multiple types of cancer, an increased frequency in myeloid-derived suppressor cells (MDSC) is associated with worse outcomes and poor therapeutic response. In the glioblastoma (GBM) microenvironment, monocytic (m) MDSCs represent the predominant subset. However, the molecular basis of mMDSC enrichment in the tumor microenvironment compared with granulocytic (g) MDSCs has yet to be determined. Here we performed the first broad epigenetic profiling of MDSC subsets to define underlying cell-intrinsic differences in behavior and found that enhanced gene accessibility of cell adhesion programs in mMDSCs is linked to their tumor-accelerating ability in GBM models upon adoptive transfer. Mouse and human mMDSCs expressed higher levels of integrin β1 and dipeptidyl peptidase-4 (DPP-4) compared with gMDSCs as part of an enhanced cell adhesion signature. Integrin β1 blockade abrogated the tumor-promoting phenotype of mMDSCs and altered the immune profile in the tumor microenvironment, whereas treatment with a DPP-4 inhibitor extended survival in preclinical GBM models. Targeting DPP-4 in mMDSCs reduced pERK signaling and their migration towards tumor cells. These findings uncover a fundamental difference in the molecular basis of MDSC subsets and suggest that integrin β1 and DPP-4 represent putative immunotherapy targets to attenuate myeloid cell-driven immune suppression in GBM.