InVivoMAb anti-mouse CD29
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$159.00 - $4,155.00
Product DetailsThe KMI6 monoclonal antibody reacts with mouse CD29 also known as integrin β1, a 120-130 kDa member of the β integrin family. CD29 is expressed by leukocytes, endothelial, smooth muscle and epithelial cells. CD29 non-covalently associates with integrin α1-α6 to form the VLA-1 through VLA-6 complexes. These α β integrin heterodimers are involved in adhesion, trafficking, proliferation and differentiation and bind to cell surface and extracellular matrix proteins including VCAM-1 and MadCAM-1.
|Isotype||Rat IgG2a, κ|
|Recommended Isotype Control(s)||InVivoMAb rat IgG2a isotype control, anti-trinitrophenol|
|Recommended Dilution Buffer||InVivoPure pH 7.0 Dilution Buffer|
|Immunogen||C57BL/6 x DBA/2 mouse bone-marrow stromal cell clone BMS2|
in vitro CD29 neutralization
PBS, pH 7.0
Contains no stabilizers or preservatives
Determined by LAL gel clotting assay
Determined by SDS-PAGE
|Sterility||0.2 μM filtered|
|Production||Purified from tissue culture supernatant in an animal free facility|
|Molecular Weight||150 kDa|
|Storage||The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.|
Recommended Isotype Control(s)
InVivoMAb rat IgG2a isotype control, anti-trinitrophenol
Recommended Dilution Buffer
InVivoPure pH 7.0 Dilution Buffer
in vitro CD29 neutralization
Bayik, D., et al. (2021). "Distinct cell adhesion signature defines glioblastoma myeloid-derived suppressor cell subsets" bioRxiv : 2021.2009.2027.461995. PubMed
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.
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.
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.
Mohammad, I., et al. (2012). "Flightless I is a focal adhesion-associated actin-capping protein that regulates cell migration" FASEB J 26(8): 3260-3272. PubMed
The role of adhesion-associated actin-binding proteins in cell migration is not well defined. In mouse fibroblasts we screened for focal adhesion-associated proteins that were isolated with collagen-coated beads and detected by tandem mass spectrometry. We identified flightless I (FliI) as an actin-binding protein in focal adhesion fractions, which was verified by immunoblotting. By confocal microscopy most FliI was distributed throughout the cytosol and in focal adhesions. By sedimentation assays and in vitro binding assays, we found that FliI associates with actin filaments and actin monomers. Assays using purified proteins showed that FliI inhibits actin polymerization and caps but does not sever actin filaments. Cells with FliI knockdown or cells overexpressing FliI migrated more or less rapidly, respectively, than wild-type controls. Compared with controls, cells with FliI knockdown were less adherent than wild-type cells, exhibited reduced numbers of focal adhesions containing activated beta1 integrins and vinculin, and exhibited increased incorporation of actin monomers into nascent filaments at focal adhesions. These data indicate that FliI regulates cell migration through its localization to focal adhesions and its ability to cap actin filaments, which collectively affect focal adhesion maturation.
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.