G-CSF ELISA Kit (DEIA-XYA993)

Regulatory status: For research use only, not for use in diagnostic procedures.

Write a review

Size
96T
Sample
cell lysates, serum, plasma
Species Reactivity
Human
Intended Use
The Human G-CSF ELISA Kit contains the components necessary for quantitative determination of natural or recombinant Human G-CSF concentrations within any experimental sample including cell lysates, serum and plasma.
Contents of Kit
1. Microstrips Coated w/ Capture Antibody: 12 x 8-Well Microcstrips
2. Protein Standard: Lyophilized (83 ng), Red
3. Biotinylated Detection Antibody: Lyophilized, Yellow
4. 400x Streptavidin-HRP: 30 μL, Blue
5. Wash Buffer (10x): 50 mL, Clear
6. Assay Diluent: 50 mL, Clear
7. Ready-to-Use Substrate: 12 mL, Brown
8. Stop Solution: 12 mL, Clear
9. Adheive Plate Sealers: 4 Seets
10. Technical Manual: 1 Manual
Storage
4°C/6 Months
Detection Range
16-2000 pg/mL
Sensitivity
The Human G-CSF ELISA Kit allows for the detection and quantification of endogenous levels of natural and/or recombinant Human G-CSF proteins within the range of 16-2000 pg/mL.
Standard Curve

Citations


Have you cited DEIA-XYA993 in a publication? Let us know and earn a reward for your research.

Customer Reviews


Write a review, share your experiences with others and get rewarded !
Product Name Cat. No. Applications Host Species Datasheet Price Add to Basket
Product Name Cat. No. Applications Host Species Datasheet Price Add to Basket

References


INFLAMMATORY SIGNATURE AFTER LOW DOSE gamma-RADIATION IN MICE BRAIN AND GUT: SWITCH FROM THERAPEUTIC BENEFIT TO INFLAMMATION

EUROPEAN JOURNAL OF INFLAMMATION

Authors: Aravindan, S.; Natarajan, M.; Veeraraghavan, J.; Herman, T. S.; Aravindan, N.

Low dose gamma-radiation (LDIR) has been used as curative/adjuvant/palliative treatment modality for a variety of medical conditions. However, LDIR has been casually linked to NF kappa B activation and inflammation. Here, we investigated the kinetics of cyto/chemokines and their influence on inflammation in normal tissues after LDIR. C57BL/6 mice exposed to LDIR (2-50cGy) and sacrificed after 1 h-8 days were examined for alterations in 95 cyto/chemokines in brain and gut (QPCR profiling) and selectively validated by assessing secreted levels (ELISA). Kinetics of LDIR-induced inflammation was assessed using DNA fragmentation and histomorphological changes in brain and gut. LDIR induced a dose-dependent upregulation of cyto/chemokines after 2-50cGy in both brain and gut. Two genes, Csf3 and Tnf alpha, were upregulated in a 'dose- and tissue-independent' manner. Transcriptional kinetics revealed induction of more genes both in brain and gut in early response time (1-48 h) after LDIR. Conversely, only few genes upregulated and more genes downregulated in these tissues after extended response (4-8 days) period. DNA fragmentation and histomorphological analysis revealed consistent dose-, time-and tissue-dependent inflammation after LDIR. Also, serum levels of TNF-alpha, VEGFA, IFN-gamma, GM-CSF, MCP-1 reinstigates the inflammatory signature after LDIR. Together, these results suggest that LDIR significantly inflicts a dose- and tissue-dependent inflammation in normal tissues and this induced inflammation may equivocate over-time and, hence frequency of LDIR use may control the switch from therapeutic benefit to inflammatory response.

Cytokine-mediated deployment of SDF-1 induces revascularization through recruitment of CXCR4(+) hemangiocytes

NATURE MEDICINE

Authors: Jin, David K.; Shido, Koji; Kopp, Hans-Georg; Petit, Isabelle; Shmelkov, Sergey V.; Young, Lauren M.; Hooper, Andrea T.; Amano, Hideki; Avecilla, Scott T.; Heissig, Beate; Hattori, Koichi; Zhang, Fan; Hicklin, Daniel J.; Wu, Yan; Zhu, Zhenping; Dunn, Ashley; Salari, Hassan; Werb, Zena; Hackett, Neil R.; Crystal, Ronald G.; Lyden, David; Rafii, Shahin

The mechanisms through which hematopoietic cytokines accelerate revascularization are unknown. Here, we show that the magnitude of cytokine-mediated release of SDF-1 from platelets and the recruitment of nonendothelial CXCR4(+)VEGFR1(+) hematopoietic progenitors, 'hemangiocytes,' constitute the major determinant of revascularization. Soluble Kit-ligand (sKitL), thrombopoietin (TPO, encoded by Thpo) and, to a lesser extent, erythropoietin (EPO) and granulocyte-macrophage colony-stimulating factor (GM-CSF) induced the release of SDF-1 from platelets, enhancing neovascularization through mobilization of CXCR4(+)VEGFR1(+) hemangiocytes. Although revascularization of ischemic hindlimbs was partially diminished in mice deficient in both GM-CSF and G-CSF (Csf2(-/-)Csf3(-/-)), profound impairment in neovascularization was detected in sKitL-deficient Mmp9(-/-) as well as thrombocytopenic Thpo(-/-) and TPO receptor-deficient (Mpl(-/-)) mice. SDF-1-mediated mobilization and incorporation of hemangiocytes into ischemic limbs were impaired in Thpo(-/-), Mpl(-/-) and Mmp9(-/-) mice. Transplantation of CXCR4(+)VEGFR1(+) hemangiocytes into Mmp9(-/-) mice restored revascularization, whereas inhibition of CXCR4 abrogated cytokine- and VEGF-A-mediated mobilization of CXCR4(+)VEGFR1(+) cells and suppressed angiogenesis. In conclusion, hematopoietic cytokines, through graded deployment of SDF-1 from platelets, support mobilization and recruitment of CXCR4(+)VEGFR1(+) hemangiocytes, whereas VEGFR1 is essential for their angiogenic competency for augmenting revascularization. Delivery of SDF- 1 may be effective in restoring angiogenesis in individuals with vasculopathies.

Online Inquiry

Name:
Phone: *
E-mail Address: *
Technology Interest:
Type of Organization:
Service & Products Interested: *
Project Description:
Verification code
Click image to refresh the verification code.

Online Inquiry

  Interested in larger quantities ? request a quote!
  Protocol may be improved. Please feel free to contact us to obtain the latest version.!

Ordering Information

Payment methods we support:
Invoice / Purchase Order
Credit card

OUR PROMISE TO YOU Guaranteed product quality expert customer support

Inquiry Basket