DLL4 Antibody [Unconjugated]

Western blot shows lysates of bEnd.3 mouse endothelioma cell line. PVDF membrane was probed with 2 µg/mL of Goat Anti-Mouse DLL4 Antigen Affinity-purified Polyclonal Antibody (Catalog # AF1389) followed by HRP-conjugated Anti-Goat IgG Secondary Antibody (Catalog # HAF017). A specific band was detected for DLL4 at approximately 90 kDa (as indicated). This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 1.

DLL4 was detected in immersion fixed bEnd.3 mouse endothelioma cell line using Goat Anti-Mouse DLL4 Antigen Affinity-purified Polyclonal Antibody (Catalog # AF1389) at 10 µg/mL for 3 hours at room temperature. Cells were stained using the NorthernLights™ 557-conjugated Anti-Goat IgG Secondary Antibody (red; Catalog # NL001) and counterstained with DAPI (blue). Specific staining was localized to cytoplasm. View our protocol for Fluorescent ICC Staining of Cells on Coverslips.

DLL4 was detected in immersion fixed paraffin-embedded sections of mouse embryo (13 d.p.c.) using Goat Anti-Mouse DLL4 Antigen Affinity-purified Polyclonal Antibody (Catalog # AF1389) at 5 µg/mL for 1 hour at room temperature followed by incubation with the Anti-Goat IgG VisUCyte™ HRP Polymer Antibody (Catalog # VC004). Tissue was stained using DAB (brown) and counterstained with hematoxylin (blue). Specific staining was localized to developing vasculature. View our protocol for IHC Staining with VisUCyte HRP Polymer Detection Reagents.

MPDZ promotes Notch signaling activity.(A) HUVECs were either transduced with lentivirus expressing GFP (sh-ctrl) or with lentivirus expressing shRNA against MPDZ (sh-MPDZ). Expression level of Notch target genes HEY1, HEY2 and HES1 were analyzed by qPCR 48 hr after transduction. Data are presented as mean ±SD. n ≥ 3; *, p<0.05; **, p<0.01; ***, p<0.001 unpaired Student’s t-test. (B) Cardiac endothelial cells were isolated from Mpdzfl/fl and Mpdz delta EC mice by magnetic beads bound with CD31 antibodies. Expression levels of Notch target genes Hey1 and Hey2 were analyzed by qPCR. Data are presented as mean ±SD. n = 3; *, p<0.05; ***, p<0.001 unpaired Student’s t-test. (C) HUVECs were either transduced with lentivirus expressing GFP (sh-ctrl) or with lentivirus expressing shRNA against MPDZ (sh-MPDZ). Expression levels of DLL1 and DLL4 were analyzed by immunoblotting 48 hr after transduction. beta -actin served as loading control. Data are presented as mean ±SD. n ≥ 3; n.s., not significant. (D) HUVECs were either transduced with adenovirus expressing GFP (ctrl) or with adenovirus expressing MPDZ. Expression levels of DLL1 and DLL4 were analyzed by immunoblotting 48 hr after transduction. beta -actin served as loading control. Data are presented as mean ±SD. n ≥ 3; n.s., not significant. (E) Lung endothelial cells were isolated from Mpdzfl/fl and Mpdz delta EC mice by CD31 magnetic beads. Protein amounts of Dll1 and Dll4 were analyzed by immunoblotting. beta -actin served as loading control. Data are presented as mean ±SD. n = 3; n.s., not significant.10.7554/eLife.32860.007Figure 2—source data 1.Source data of qantitative PCR analysis related to Figure 2A and B.Source data of qantitative PCR analysis related to Figure 2A and B. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/29620522), licensed under a CC-BY license. Not internally tested by R&D Systems.

Mpdz does not affect cell cell junction assembly.(A, B) HUVECs were either transduced with lentivirus expressing GFP (sh-ctrl) or with lentivirus expressing shRNA against MPDZ (sh-MPDZ). Cells were cultured under sparse conditions (A) or confluent conditions (B). After PFA fixation cells were stained for DLL1 and Nectin-2 or DLL4 and Nectin-2 and counterstained with DAPI. Images were acquired with the confocal microscope LSM 700. Arrow indicates co-localization of DLL1/4 with Nectin-2 at the cell membrane. Arrow head indicates diminished co-localization at the cell membrane. Scale bar: 10 µm. (C) HUVECs were either transfected with control siRNA (si-ctrl) or with siRNA against Nectin-2 (si-Nectin-2). After PFA fixation cells were stained for DLL1 and Nectin-2 or DLL4 and Nectin-2. Images were acquired with the confocal microscope LSM 700. Arrow indicates localization of DLL1/4 at the cell membrane.Scale bar: 10 µm. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/29620522), licensed under a CC-BY license. Not internally tested by R&D Systems.

MPDZ promotes Notch signaling activity.(A) HUVECs were either transduced with lentivirus expressing GFP (sh-ctrl) or with lentivirus expressing shRNA against MPDZ (sh-MPDZ). Expression level of Notch target genes HEY1, HEY2 and HES1 were analyzed by qPCR 48 hr after transduction. Data are presented as mean ±SD. n ≥ 3; *, p<0.05; **, p<0.01; ***, p<0.001 unpaired Student’s t-test. (B) Cardiac endothelial cells were isolated from Mpdzfl/fl and Mpdz delta EC mice by magnetic beads bound with CD31 antibodies. Expression levels of Notch target genes Hey1 and Hey2 were analyzed by qPCR. Data are presented as mean ±SD. n = 3; *, p<0.05; ***, p<0.001 unpaired Student’s t-test. (C) HUVECs were either transduced with lentivirus expressing GFP (sh-ctrl) or with lentivirus expressing shRNA against MPDZ (sh-MPDZ). Expression levels of DLL1 and DLL4 were analyzed by immunoblotting 48 hr after transduction. beta -actin served as loading control. Data are presented as mean ±SD. n ≥ 3; n.s., not significant. (D) HUVECs were either transduced with adenovirus expressing GFP (ctrl) or with adenovirus expressing MPDZ. Expression levels of DLL1 and DLL4 were analyzed by immunoblotting 48 hr after transduction. beta -actin served as loading control. Data are presented as mean ±SD. n ≥ 3; n.s., not significant. (E) Lung endothelial cells were isolated from Mpdzfl/fl and Mpdz delta EC mice by CD31 magnetic beads. Protein amounts of Dll1 and Dll4 were analyzed by immunoblotting. beta -actin served as loading control. Data are presented as mean ±SD. n = 3; n.s., not significant.10.7554/eLife.32860.007Figure 2—source data 1.Source data of qantitative PCR analysis related to Figure 2A and B.Source data of qantitative PCR analysis related to Figure 2A and B. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/29620522), licensed under a CC-BY license. Not internally tested by R&D Systems.

Endothelial changes after pericyte depletion. a–f Maximum intensity projection of confocal images from control and DTRiPC P6 retinas stained for IB4 (red) in combination with VEGF-A a, VEGFR2 b, VEGFR3 c, Tie2 d, Esm1 e, and Dll4 f (all in white), as indicated. Note local increase of VEGFR2, VEGFR3, and Esm1 (arrowheads in b, c, e) but not Tie2 or VEGF-A at the edge of the vessel plexus. Dll4 expression in DTRiPC sprouts is increased in some regions (arrowheads) but absent in others (arrows). Scale bar, 100 µm. g–j Quantitation of VEGF-A immunosignals area and intensity g, signal intensity for VEGFR2 h and VEGFR3 i and proportion of Esm1+ area with respect to vascular area j in the P6 control and DTRiPC angiogenic front. Error bars, s.e.m. p-values, Student’s t-test. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/29146905), licensed under a CC-BY license. Not internally tested by R&D Systems.

Targeting of Fbxw7 induced the upregulation of Dll4 expression.Anti-Dll4 and Isolectin B4 (IsolB4)-stained retinal whole-mounts of Fbxw7iECKO and littermate control retinas, as indicated (A, B). Arrowheads in (B) mark Dll4+ peripheral sprouts at the edge of the growing plexus, arrows indicate upregulated Dll4 in Fbxw7iECKO retinal capillaries. Quantitative analysis (with Volocity 5; n = 3 for each group) of image data confirmed elevated Dll4 levels (number of pixels) in the mutant endothelium (C). Likewise, quantitative RT-PCR analysis showed reduced Fbxw7 expression but upregulated Dll4 transcript levels in P6 Fbxw7iECKO lungs (D). Expression of the Cdh5 gene was used for normalization. Error bars indicate SEM. P values are indicated as ** (<0.001) and * (p<0.05). Scale bars are 100 µm. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/22848434), licensed under a CC-BY license. Not internally tested by R&D Systems.

Targeting of Fbxw7 induced the upregulation of Dll4 expression.Anti-Dll4 and Isolectin B4 (IsolB4)-stained retinal whole-mounts of Fbxw7iECKO and littermate control retinas, as indicated (A, B). Arrowheads in (B) mark Dll4+ peripheral sprouts at the edge of the growing plexus, arrows indicate upregulated Dll4 in Fbxw7iECKO retinal capillaries. Quantitative analysis (with Volocity 5; n = 3 for each group) of image data confirmed elevated Dll4 levels (number of pixels) in the mutant endothelium (C). Likewise, quantitative RT-PCR analysis showed reduced Fbxw7 expression but upregulated Dll4 transcript levels in P6 Fbxw7iECKO lungs (D). Expression of the Cdh5 gene was used for normalization. Error bars indicate SEM. P values are indicated as ** (<0.001) and * (p<0.05). Scale bars are 100 µm. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/22848434), licensed under a CC-BY license. Not internally tested by R&D Systems.

DLL4 expressed from the Dll1 locus rescues DLL1 loss-of-function in the retina.(A)Dll1 null mutant retinas show epithelial disruption with formation of polarised rosettes in which the apical markers N-Cadherin (NCad, a) and ZO-1 (ZO1, b) are abnormally present at the central lumen. Ectopic proliferating progenitors, labelled with PHH3 (b, arrowheads), are located close to the apical lumen of these rosettes. (B) In contrast, the neuroepithelium of homozygous Dll1Dll1ki and Dll1Dll4ki embryos is correctly organised without rosettes, and N-Cadherin shows the normal apical localisation close to the retinal pigmented epithelium (a,b). Mitotic progenitors (PHH3+) are only detected at the apical region of the neuroepithelium (a,b arrowheads). A normal stratification of CHX10+ progenitors and P27+ differentiating neurons is also observed (c,d). (C, D) E13.5 homozygous Dll1Dll1ki and Dll1Dll4ki retinas show no significant difference in the number of ISL1+ RGCs (C) and CRABP+ amacrine cells (D). Cells immunopositive for Islet-1 and Crabp were counted and related to the total number of cells in the retina (DAPI+). Percentages are shown as mean ± SEM; ns, not significant. (E) Expression of DLL4 in homozygous Dll1Dll1ki (a,c) and in homozygous Dll1Dll4ki (b,d) E13.5 retinas as detected by an anti-DLL4 antibody. (c) and (d) are magnifications of (a) and (b), respectively. Endogenous plus transgenic DLL4 is expressed in more cells in Dll1Dll4ki/Dll4ki as compared to endogenous DLL4 expression in Dll1Dll1ki/Dll1ki while signal strength is similar. Scale bars are 50 μm in (A, B) and 100 μm in (E). Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/26114479), licensed under a CC-BY license. Not internally tested by R&D Systems.

Dll1 and Dll4 are expressed in distinct patterns in the mice gastrointestinal epithelium.Immunohistochemistry of Dll1 and Dll4 were performed using mice small intestinal (A, B) and colonic tissues (D, E). Within the small intestinal epithelium, staining by anti-Dll1 antibody showed positive cells exclusively within the crypt (A, B), whereas staining by anti-Dll4 antibody showed positive cells both in the crypt and in the villi. Quantification of Dll1+ve and Dll4+ve intestinal epithelial cells (IECs) showed that Dll1+ve IECs are predominantly found within the crypt, whereas Dll4+ve IECs are found mostly in the villi (C). In the colonic epithelium, staining by anti-Dll1 antibody showed positive cells exclusively within the lower part of the crypt (D, E), whereas staining by anti-Dll4 antibody showed positive cells both in the lower- and upper part of the crypt, including the surface epithelium. Quantification of Dll1+ve and Dll4+ve IECs showed that Dll1+ve IECs are found exclusively within the lower half of the crypt, whereas Dll4+ve IECs are found both in the lower and upper region of the crypt at a comparable frequency (F). Negative staining of non-immunized isotype antibodies (Control Ab) confirmed the specific staining of Dll1 (A) and Dll4 (D). Scale bar represents 20 µm. Quantitative data are shown as mean ∓ SD of triplicate experiments (n = 3). ∗ indicates P < 0.05 as determined by Welch’s t-test. N.S. indicates not significant. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/24860699), licensed under a CC-BY license. Not internally tested by R&D Systems.

Dll1+ve or Dll4+ve IECs constitute the intestinal stem cell niche.Double immunostaining of Dll1 or Dll4 with a stem-cell niche cell marker, Lysozyme or c-kit, was performed in the mice small intestine and in the colon, respectively. (A) Immunostaining of Dll4 (green) with Lysozyme (red) shows that Dll4 is expressed in Paneth cells of the small intestine (yellow arrowhead). Scale bar represents 20 µm. (B) Double immunostaining of Dll1 (green) and c-kit (red) shows that Dll1+ve colonic IECs mostly co-express c-kit (yellow arrowhead). Also, double immunostaining of Dll4 (green) and c-kit (red) showed that a distinct population of Dll4+ve cells co-express c-kit (yellow arrowhead). Scale bar represents 20 µm. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/24860699), licensed under a CC-BY license. Not internally tested by R&D Systems.

Dll1+ve or Dll4+ve IECs constitute the intestinal stem cell niche.Double immunostaining of Dll1 or Dll4 with a stem-cell niche cell marker, Lysozyme or c-kit, was performed in the mice small intestine and in the colon, respectively. (A) Immunostaining of Dll4 (green) with Lysozyme (red) shows that Dll4 is expressed in Paneth cells of the small intestine (yellow arrowhead). Scale bar represents 20 µm. (B) Double immunostaining of Dll1 (green) and c-kit (red) shows that Dll1+ve colonic IECs mostly co-express c-kit (yellow arrowhead). Also, double immunostaining of Dll4 (green) and c-kit (red) showed that a distinct population of Dll4+ve cells co-express c-kit (yellow arrowhead). Scale bar represents 20 µm. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/24860699), licensed under a CC-BY license. Not internally tested by R&D Systems.

MPDZ promotes Notch signaling activity.(A) HUVECs were either transduced with lentivirus expressing GFP (sh-ctrl) or with lentivirus expressing shRNA against MPDZ (sh-MPDZ). Expression level of Notch target genes HEY1, HEY2 and HES1 were analyzed by qPCR 48 hr after transduction. Data are presented as mean ±SD. n ≥ 3; *, p<0.05; **, p<0.01; ***, p<0.001 unpaired Student’s t-test. (B) Cardiac endothelial cells were isolated from Mpdzfl/fl and Mpdz delta EC mice by magnetic beads bound with CD31 antibodies. Expression levels of Notch target genes Hey1 and Hey2 were analyzed by qPCR. Data are presented as mean ±SD. n = 3; *, p<0.05; ***, p<0.001 unpaired Student’s t-test. (C) HUVECs were either transduced with lentivirus expressing GFP (sh-ctrl) or with lentivirus expressing shRNA against MPDZ (sh-MPDZ). Expression levels of DLL1 and DLL4 were analyzed by immunoblotting 48 hr after transduction. beta -actin served as loading control. Data are presented as mean ±SD. n ≥ 3; n.s., not significant. (D) HUVECs were either transduced with adenovirus expressing GFP (ctrl) or with adenovirus expressing MPDZ. Expression levels of DLL1 and DLL4 were analyzed by immunoblotting 48 hr after transduction. beta -actin served as loading control. Data are presented as mean ±SD. n ≥ 3; n.s., not significant. (E) Lung endothelial cells were isolated from Mpdzfl/fl and Mpdz delta EC mice by CD31 magnetic beads. Protein amounts of Dll1 and Dll4 were analyzed by immunoblotting. beta -actin served as loading control. Data are presented as mean ±SD. n = 3; n.s., not significant.10.7554/eLife.32860.007Figure 2—source data 1.Source data of qantitative PCR analysis related to Figure 2A and B.Source data of qantitative PCR analysis related to Figure 2A and B. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/29620522), licensed under a CC-BY license. Not internally tested by R&D Systems.

• Reactivity: Mu
• Applications: WB, IHC, ICC/IF
• Clonality: Polyclonal
• Host: Goat
• Conjugate: Unconjugated
• Concentration: LYOPH

DLL4 Antibody [Unconjugated] Summary

• Immunogen: Mouse myeloma cell line NS0-derived recombinant mouse DLL4
  Ser28-Pro525
  Accession # BAB18580
• Specificity: Detects mouse DLL4 in direct ELISAs and Western blots. In direct ELISAs, approximately 50% cross-reactivity with recombinant human DLL4 is observed.
• Source: N/A
• Isotype: IgG
• Clonality: Polyclonal
• Host: Goat
• Gene: DLL4
• Purity Statement: Antigen Affinity-purified

Applications/Dilutions

• Dilutions:
  • Immunocytochemistry 5-15 ug/mL
  • Immunohistochemistry 5-15 ug/mL
  • Western Blot 2 ug/mL

Packaging, Storage & Formulations

• Storage: Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
  12 months from date of receipt, -20 to -70 degreesC as supplied. 1 month, 2 to 8 degreesC under sterile conditions after reconstitution. 6 months, -20 to -70 degreesC under sterile conditions after reconstitution.
• Buffer: Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. *Small pack size (SP) is supplied either lyophilized or as a 0.2 µm filtered solution in PBS.
• Preservative: No Preservative
• Concentration: LYOPH
• Reconstitution Instructions: Reconstitute at 0.2 mg/mL in sterile PBS.

Notes

This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.

Alternate Names for DLL4 Antibody [Unconjugated]

• Delta 4 precursor
• delta 4
• delta ligand 4
• delta4
• delta-like 4 (Drosophila)
• delta-like 4 homolog (Drosophila)
• delta-like 4 homolog
• delta-like 4 protein
• delta-like protein 4
• DLL4
• Drosophila Delta homolog 4
• hdelta2
• MGC126344
• notch ligand delta-2
• notch ligand DLL4

Background

Delta-Like protein 4 (DLL4) is a type I membrane protein belonging to the Delta/Serrate/Lag2 (DSL) family of Notch ligands (1). Notch signaling is an evolutionarily conserved pathway that controls cell fate and is required in multiple developmental processes including vascular development, hematopoiesis, somatogenesis, myogenesis, and neurogenesis (2-4). Dysregulation in the Notch pathway is associated with various human diseases. In mammals, four Notch homologs (Notch 1 to 4) and five ligands (DLL 1, 3 and 4, Jagged 1 and 2) have been identified. Notch ligands are transmembrane proteins with a DSL motif necessary for Notch binding, tandem EGF repeats, a transmembrane region and a short intracellular domain (ICD). Notch ligands are categorized into two subfamilies based on the presence of an extracellular cysteine-rich domain and insertions that interrupt some EGF repeats in the Jagged but not the Delta ligand family. Interactions of Notch receptors with their ligands results in reciprocal Regulated Intramembrane Proteolysis (RIP) (4). RIP is a mechanism for transmembrane signal transduction that involves the sequential processing by A Disintegrin Metalloprotease (ADAM) and then by Presenilin/ gamma -Ssecretase, resulting in shedding of the extracellular domains and the generation of the soluble ICD signaling fragments, respectively. The Notch ICD translocates to the nucleus and interacts with transcriptional coactivators, resulting in the transcription of target genes. The ICDs of the Notch ligands have also been shown to translocate to the nucleus where they may have a signaling function (5, 6). DLL4 is expressed highly and selectively within the arterial endothelium and has been shown to function as a ligand for Notch 1 and Notch 4. Human and mouse DLL4 share 86% amino acid sequence identity (1).

1. Shutter, J.R. et al. (2000) Genes Dev. 14:1313.
2. Iso, Tatsuya et al. (2002) Arterioscler. Thromb. Vasc. Biol. 23:543.
3. Walker, L. et al. (2001) Stem Cells 19:543.
4. Baron, M. (2002) Semin. Cell Dev. Biol. 14:113.
5. Ikeuchi, T. and S.S. Sisodia (2003) J. Biol. Chem. 278:7751.
6. Bland, C.E. et al. (2003) J. Biol. Chem. 278:13607.

Limitations

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

Publications for DLL4 Antibody (AF1389)(65)

Publications using AF1389

• Mu, Y;Hu, S;Liu, X;Tang, X;Lin, J;Shi, H; Mechanical forces pattern endocardial Notch activation via mTORC2-PKC pathway eLife 2025-02-11 [PMID: 39932433] (Immunohistochemistry, Mouse)
• Mohanakrishnan, V;Sivaraj, KK;Jeong, HW;Bovay, E;Dharmalingam, B;Bixel, MG;Dinh, VV;Petkova, M;Paredes Ugarte, I;Kuo, YT;Gurusamy, M;Raftrey, B;Chu, NTL;Das, S;Rios Coronado, PE;Stehling, M;Sävendahl, L;Chagin, AS;Mäkinen, T;Red-Horse, K;Adams, RH; Specialized post-arterial capillaries facilitate adult bone remodelling Nature cell biology 2024-11-11 [PMID: 39528700] (Immunohistochemistry, Transgenic Mouse)
• Ren, JS;Bai, W;Ding, JJ;Ge, HM;Wang, SY;Chen, X;Jiang, Q; Hypoxia-induced AFAP1L1 regulates pathological neovascularization via the YAP-DLL4-NOTCH axis Journal of translational medicine 9/22/2023 [PMID: 37737201]
• Bai, W;Ren, JS;Xia, M;Zhao, Y;Ding, JJ;Chen, X;Jiang, Q; Targeting FSCN1 with an oral small-molecule inhibitor for treating ocular neovascularization Journal of translational medicine 2023-08-18 [PMID: 37596693] (IHC, Mouse)
• Biswas, S;Shahriar, S;Bachay, G;Arvanitis, P;Brunken, WJ;Agalliu, D; Glutamatergic neuronal activity regulates angiogenesis and blood-retinal barrier maturation via Norrin/ beta -catenin signaling bioRxiv : the preprint server for biology 2023-07-11 [PMID: 37503079] (IHC, Transgenic Mouse, Mouse)
• EM Davies, R Gurung, KQ Le, KTT Roan, RP Harvey, GM Mitchell, Q Schwarz, CA Mitchell PI(4,5)P2-dependent regulation of endothelial tip cell specification contributes to angiogenesis Science Advances, 2023-03-31;9(13):eadd6911. 2023-03-31 [PMID: 37000875] (IHC, Mouse)
• Q Hou, J Jia, J Lin, L Zhu, S Xie, Q Yu, Y Li Bacillus subtilis programs the differentiation of intestinal secretory lineages to inhibit Salmonella infection Cell Reports, 2022-09-27;40(13):111416. 2022-09-27 [PMID: 36170821] (Western Blot, Mouse)
• Raghu Ram Katreddi, Ed Zandro M. Taroc, Sawyer M. Hicks, Jennifer M. Lin, Shuting Liu, Mengqing Xiang et al. Notch signaling determines cell-fate specification of the two main types of vomeronasal neurons of rodents Development 2022-07-01 [PMID: 35781337] (Immunohistochemistry, Mouse)
• JH Bae, MJ Yang, SH Jeong, J Kim, SP Hong, JW Kim, YH Kim, GY Koh Gatekeeping role of Nf2/Merlin in vascular tip EC induction through suppression of VEGFR2 internalization Science Advances, 2022-06-10;8(23):eabn2611. 2022-06-10 [PMID: 35687678] (IHC, Mouse)
• Choong-kun Lee, Bo-Yoon Park, Taehee Jo, Cheol-Heum Park, Ju-Hee Kim, Kyu-Jin Chung et al. Dll4 Inhibition Promotes Graft Retention in Fat Grafting Enriched with Adipose-Derived Stem Cells Stem Cells Translational Medicine 2022-07-20 [PMID: 35579982]
• C Xu, VV Dinh, K Kruse, HW Jeong, EC Watson, S Adams, F Berkenfeld, M Stehling, SJ Rasouli, R Fan, R Chen, I Bedzhov, Q Chen, K Kato, ME Pitulescu, RH Adams Induction of osteogenesis by bone-targeted Notch activation Elife, 2022-02-04;11(0):. 2022-02-04 [PMID: 35119364] (IHC, Western Blot, Mouse)
• E Azzoni, V Frontera, G Anselmi, C Rode, C James, EM Deltcheva, AS Demian, J Brown, C Barone, A Patelli, JR Harman, M Nicholls, SJ Conway, E Morrissey, SEW Jacobsen, DB Sparrow, AL Harris, T Enver, MFTR de Bruijn The onset of circulation triggers a metabolic switch required for endothelial to hematopoietic transition Cell Reports, 2021-12-14;37(11):110103. 2021-12-14 [PMID: 34910918] (IHC, Mouse, Transgenic Mouse)
• Guofu Zhu, Ying Lin, Tandi Ge, Shekhar Singh, Hao Liu, Linlin Fan et al. A novel peptide inhibitor of Dll4‐Notch1 signalling and its pro‐angiogenic functions British Journal of Pharmacology 2022-04-01 [PMID: 34796471]
• Su W, Sun S, Tian B et al. Efficacious, safe and stable inhibition of corneal neovascularization by AAV vectored anti-VEGF therapeutics Mol Ther Methods Clin Dev 9/13/2021 [PMID: 34514023]
• Georgia Zarkada, Joel P. Howard, Xue Xiao, Hyojin Park, Mathilde Bizou, Severine Leclerc et al. Specialized endothelial tip cells guide neuroretina vascularization and blood-retina-barrier formation Developmental Cell 2021-08-01 [PMID: 34273276] (Immunohistochemistry, Transgenic Mouse)
• Ri Yu, Nam-Suk Kim, Yan Li, Jin-Young Jeong, Sang-Joon Park, Bin Zhou et al. Vascular Sema3E-Plexin-D1 Signaling Reactivation Promotes Post-stroke Recovery through VEGF Downregulation in Mice Translational Stroke Research 2022-02-01 [PMID: 33978913]
• DH Yeom, YS Lee, I Ryu, S Lee, B Sung, HB Lee, D Kim, JH Ahn, E Ha, YS Choi, SH Lee, WK You ABL001, a Bispecific Antibody Targeting VEGF and DLL4, with Chemotherapy, Synergistically Inhibits Tumor Progression in Xenograft Models International Journal of Molecular Sciences, 2020-12-29;22(1):. 2020-12-29 [PMID: 33383646] (IHC, Mouse)
• G Sharma, JM Jagtap, AK Parchur, VR Gogineni, S Ran, C Bergom, SB White, MJ Flister, A Joshi Heritable modifiers of the tumor microenvironment influence nanoparticle uptake, distribution and response to photothermal therapy Theranostics, 2020-04-06;10(12):5368-5383. 2020-04-06 [PMID: 32373218] (IHC, Rat)
• C Viallard, C Audiger, N Popovic, N Akla, K Lanthier, I Legault-Na, H Melichar, S Costantino, S Lesage, B Larrivée BMP9 signaling promotes the normalization of tumor blood vessels Oncogene, 2020-02-10;0(0):. 2020-02-10 [PMID: 32042114] (Western Blot, Human)
• R Fu, WC Lv, Y Xu, MY Gong, XJ Chen, N Jiang, Y Xu, QQ Yao, L Di, T Lu, LM Wang, R Mo, ZQ Wu Endothelial ZEB1 promotes angiogenesis-dependent bone formation and reverses osteoporosis Nat Commun, 2020-01-23;11(1):460. 2020-01-23 [PMID: 31974363] (IHC, Mouse)
• Jie Gao, Michael Van Meter, Susana Hernandez Hernandez Lopez, Guoying Chen, Ying Huang, Shumei Ren et al. Therapeutic targeting of Notch signaling and immune checkpoint blockade in a spontaneous, genetically-heterogeneous mouse model of T-cell acute lymphoblastic leukemia Disease Models & Mechanisms 2019-09-01 [PMID: 31399482] (Immunohistochemistry, Mouse)
• D Yasuda, D Kobayashi, N Akahoshi, T Ohto-Nakan, K Yoshioka, Y Takuwa, S Mizuno, S Takahashi, S Ishii Lysophosphatidic acid-induced YAP/TAZ activation promotes developmental angiogenesis by repressing Notch ligand Dll4 J. Clin. Invest., 2019-07-23;130(0):. 2019-07-23 [PMID: 31335323] (IHC, Mouse)
• S Payne, M Gunadasa-R, A Neal, AN Redpath, J Patel, KM Chouliaras, I Ratnayaka, N Smart, S De Val Regulatory pathways governing murine coronary vessel formation are dysregulated in the injured adult heart Nat Commun, 2019-07-22;10(1):3276. 2019-07-22 [PMID: 31332177] (IHC-Fr, Mouse)
• Z Gong, B Shang, Y Chu, X Chen, Q Li, K Liu, Y Chen, Y Huang, Y Han, Q Shang, Z Zheng, L Song, Y Li, R Liu, C Xu, X Zhang, B Liu, L Wang, C Shao, Y Wang, Y Shi Fibrotic liver microenvironment promotes Dll4 and SDF-1-dependent T-cell lineage development Cell Death Dis, 2019-06-05;10(6):440. 2019-06-05 [PMID: 31165736] (IHC, Human, Mouse)
• M Fernández-, V Casquero-G, W Luo, F Francesca, S Ferreira R, S Del Olmo-C, R Benedito iSuRe-Cre is a genetic tool to reliably induce and report Cre-dependent genetic modifications Nat Commun, 2019-05-22;10(1):2262. 2019-05-22 [PMID: 31118412] (IHC-F, Mouse)
• A Neal, S Nornes, S Payne, MD Wallace, M Fritzsche, P Louphrasit, RN Wilkinson, KM Chouliaras, K Liu, K Plant, R Sholapurka, I Ratnayaka, W Herzog, G Bond, T Chico, G Bou-Ghario, S De Val Venous identity requires BMP signalling through ALK3 Nat Commun, 2019-01-28;10(1):453. 2019-01-28 [PMID: 30692543] (IHC, Mouse)
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Review for DLL4 Antibody (AF1389) (1)

Average Rating: 3

(Based on 1 review)

We have 1 review tested in 1 species: Mouse.

reviewed by: Verified Customer ICC Mouse 01/05/2015

Summary

• Application: Immunocytochemistry
• Sample Tested: See PMID 23091063
• Species: Mouse

Bioinformatics

• Gene Symbol: DLL4
• Uniprot:
  • BAB18580()