Ultra-LEAF™ Purified anti-human CCL27 (CTACK) Antibody, A15094F,BioLegend,940304

Host

Mouse

Reactivity

Human

Application

Neut - Quality tested

Platform ID

BAB671856878

BioLegend

Headquarters

8999 BioLegend Way San Diego, CA 92121 United States

Contact

Tel: 1-858-455-9588
Fax: +49 (4131) 7023913

Email:

Product Specifications
Scientific Background

Specifications

NameUltra-LEAF™ Purified anti-human CCL27 (CTACK) Antibody, A15094F
Cat. No.940304
HostMouse
RRIDAB_2894526 (BioLegend Cat. No. 940303)AB_2894526 (BioLegend Cat. No. 940304)
IsotypeMouse IgG2b, κ
ReactivityHuman
ApplicationNeut - Quality tested
ClonalityMonoclonal
Clone NumberA15094F
ConcentrationThe antibody is bottled at the concentration indicated on the vial, typically between 2 mg/mL and 3 mg/mL. Older lots may have also been bottled at 1 mg/mL. To obtain lot-specific concentration and expiration, please enter the lot number in ourCertificate of Analysisonline tool.
TargetCCL27
ImmunogenRecombinant human CCL27 (CTACK)
PurityThe Ultra-LEAF™ (Low Endotoxin, Azide-Free) antibody was purified by affinity chromatography.
Formulation0.2 µm filtered in phosphate-buffered solution, pH 7.2, containing no preservative.
StorageThe antibody solution should be stored undiluted between 2°C and 8°C. This Ultra-LEAF™ solution contains no preservative; handle under aseptic conditions.
Regulatory StatusResearch Use Only

Scientific Background

CCL27 is highly expressed in skin where it is constitutively produced by keratinocytes. CCL27 binds to CCR10 (shared with CCL28) which is expressed on melanocytes, fibroblasts, and dermal microvascular endothelial cells. The interaction of CCL27 with CCR10 has a main role in skin homeostasis and inflammation. It has been described that more than 90% of the lymphocytes in the skin of patients with psoriasis, atopic dermatitis, and allergic-contact dermatitis express CCR10. In melanoma, CCR10 increases the ability of neoplastic cells to grow, invade tissues, disseminate to lymph nodes, and escape host immune responses. Also, it has been described that human skin tumors elude T cell-mediated antitumor immune responses by down-regulating the expression of CCL27. Interestingly, this down-regulation is mediated by EGFR signaling. In addition, CCL27 upregulation in melanoma cells impairs tumor growth due to the recruitment and accumulation of T cells and natural killer cells at tumor sites, resulting in enhanced antitumor immune responses.

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