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Jagged1 (H-114) antibody


Antibody ID


Target Antigen

Jagged1 (H-114) mouse, rat, human, rat, mouse

Proper Citation

(Santa Cruz Biotechnology Cat# sc-8303, RRID:AB_649685)


polyclonal antibody


Discontinued: 2016; validation status unknown check with seller; recommendations: Immunoprecipitation; Western Blot; Immunocytochemistry; ELISA; Immunofluorescence; Immunohistochemistry; WB, IP, IF, IHC(P), ELISA

Host Organism



Santa Cruz Biotechnology

Cat Num


Publications that use this research resource

Therapeutic Antibody Targeting Tumor- and Osteoblastic Niche-Derived Jagged1 Sensitizes Bone Metastasis to Chemotherapy.

  • Zheng H
  • Cancer Cell
  • 2017 Dec 11

Literature context:


Bone metastasis is a major health threat to breast cancer patients. Tumor-derived Jagged1 represents a central node in mediating tumor-stromal interactions that promote osteolytic bone metastasis. Here, we report the development of a highly effective fully human monoclonal antibody against Jagged1 (clone 15D11). In addition to its inhibitory effect on bone metastasis of Jagged1-expressing tumor cells, 15D11 dramatically sensitizes bone metastasis to chemotherapy, which induces Jagged1 expression in osteoblasts to provide a survival niche for cancer cells. We further confirm the bone metastasis-promoting function of osteoblast-derived Jagged1 using osteoblast-specific Jagged1 transgenic mouse model. These findings establish 15D11 as a potential therapeutic agent for the prevention or treatment of bone metastasis.

Funding information:
  • NCI NIH HHS - P30 CA072720()
  • NCI NIH HHS - R01 CA134519()
  • NCI NIH HHS - R01 CA141062()
  • NCI NIH HHS - R01 CA212410()
  • NIGMS NIH HHS - R29 GM053989(United States)

Lunatic fringe-mediated Notch signaling regulates adult hippocampal neural stem cell maintenance.

  • Semerci F
  • Elife
  • 2017 Jul 12

Literature context:


Hippocampal neural stem cells (NSCs) integrate inputs from multiple sources to balance quiescence and activation. Notch signaling plays a key role during this process. Here, we report that Lunatic fringe (Lfng), a key modifier of the Notch receptor, is selectively expressed in NSCs. Further, Lfng in NSCs and Notch ligands Delta1 and Jagged1, expressed by their progeny, together influence NSC recruitment, cell cycle duration, and terminal fate. We propose a new model in which Lfng-mediated Notch signaling enables direct communication between a NSC and its descendants, so that progeny can send feedback signals to the 'mother' cell to modify its cell cycle status. Lfng-mediated Notch signaling appears to be a key factor governing NSC quiescence, division, and fate.

Funding information:
  • NCI NIH HHS - P30 CA125123()
  • NCRR NIH HHS - S10 RR024574()
  • NIAID NIH HHS - P30 AI036211()
  • NICHD NIH HHS - U54 HD083092()
  • NIDCD NIH HHS - R01 DC006185()
  • NIDCD NIH HHS - R01 DC014832()
  • NIH HHS - S10 OD016167()

Fine-tuning of Notch signaling sets the boundary of the organ of Corti and establishes sensory cell fates.

  • Basch ML
  • Elife
  • 2016 Dec 14

Literature context:


The signals that induce the organ of Corti and define its boundaries in the cochlea are poorly understood. We show that two Notch modifiers, Lfng and Mfng, are transiently expressed precisely at the neural boundary of the organ of Corti. Cre-Lox fate mapping shows this region gives rise to inner hair cells and their associated inner phalangeal cells. Mutation of Lfng and Mfng disrupts this boundary, producing unexpected duplications of inner hair cells and inner phalangeal cells. This phenotype is mimicked by other mouse mutants or pharmacological treatments that lower but not abolish Notch signaling. However, strong disruption of Notch signaling causes a very different result, generating many ectopic hair cells at the expense of inner phalangeal cells. Our results show that Notch signaling is finely calibrated in the cochlea to produce precisely tuned levels of signaling that first set the boundary of the organ of Corti and later regulate hair cell development.

Funding information:
  • NIDCD NIH HHS - R01 DC004189()
  • NIDCD NIH HHS - R01 DC006185()
  • NIDCD NIH HHS - R01 DC011571()

Notch signaling plays a critical role in motility and differentiation of human first-trimester cytotrophoblasts.

  • Haider S
  • Endocrinology
  • 2014 Jan 24

Literature context:


Failures in human extravillous trophoblast (EVT) development could be involved in the pathogenesis of pregnancy diseases. However, the underlying mechanisms have been poorly characterized. Here, we provide evidence that Notch signaling could represent a key regulatory pathway controlling trophoblast proliferation, motility, and differentiation. Immunofluorescence of first-trimester placental tissues revealed expression of Notch receptors (Notch2 and Notch3) and membrane-anchored ligands (delta-like ligand [DLL] 1 and -4 and Jagged [JAG] 1 and -2) in villous cytotrophoblasts (vCTBs), cell column trophoblasts (CCTs), and EVTs. Notch4 and Notch1 were exclusively expressed in vCTBs and in CCTs, respectively. Both proteins decreased in Western blot analyses of first-trimester, primary cytotrophoblasts (CTBs) differentiating on fibronectin. Luciferase reporter analyses suggested basal, canonical Notch activity in SGHPL-5 cells and primary cells that was increased upon seeding on DLL4-coated dishes and diminished in the presence of the Notch/γ-secretase inhibitors N-[N-(3,5-difluorophenacetyl-l-alanyl)]-S-phenylglycine t-butyl ester (DAPT) or L-685,458. Bromodeoxyuridine labeling, cyclin D1 mRNA expression, and cell counting indicated that chemical inhibition of Notch signaling elevated proliferation in the different primary trophoblast model systems. Notch inhibition also increased motility of SGHPL-5 cells through uncoated and fibronectin-coated Transwells, motility of primary CTBs, as well as migration in villous explant cultures on collagen I. Accordingly, small interfering RNA-mediated gene silencing of Notch1 also elevated SGHPL-5 cell migration. In contrast, motility of primary cultures and SGHPL-5 cells was diminished in the presence of DLL4. Moreover, DAPT increased markers of differentiated EVT, ie, human leukocyte antigen G1, integrin α5, and T-cell factor 4, whereas DLL4 provoked the opposite. In summary, the data suggest that canonical Notch signaling impairs motility and differentiation of first-trimester CTBs.

Funding information:
  • NIEHS NIH HHS - R01 ES013143(United States)
  • NIMHD NIH HHS - G12 MD007592(United States)