Anti-IL-9 Mouse mAb

ArtNr	PTM-6138
Hersteller	PTM Biolabs
Menge	100 ul
Kategorie	Antibodies Primary Antibodies
Typ	Antibody Monoclonal
Format	Lyophilized powder
Applikationen	FC
Clon	10258
Specific against	Human (Homo sapiens)
Host	Mouse
Isotype	IgG1
Konjugat/Tag	Unconjugated
ECLASS 10.1	42030590
ECLASS 11.0	42030590
UNSPSC	12352203
Alias	Cytokine P40,T-cell growth factor P40
Versandbedingung	Raumtemperatur
Lieferbar
Manufacturer - Type	Primary Antibodies
Manufacturer - Category	Uncategorized
Manufacturer - Targets	IL-9
Shipping Temperature	Ambient temperature
Storage Conditions	Store at -20°C. Avoid freeze/thaw cycles.
Stability	Stable for 12 months from date of receipt/reconstitution.
Manufacturer - Research Area	Immunology, Cancer
Product description	IL-9 is a cytokine secreted by CD4+ helper cells that acts as a regulator of a variety of hematopoietic cells. IL-9 stimulates cell proliferation and prevents apoptosis. It functions through the interleukin-9 receptor (IL9R), which activates different signal transducer and activator (STAT) proteins namely STAT1, STAT3 and STAT5. The gene encoding IL-9 has been identified as a candidate gene for asthma. Genetic studies on a mouse model of asthma demonstrated that IL-9 is a determining factor in the pathogenesis of bronchial hyperresponsiveness.
Purification Method	Protein G purified
Formula	PBS, Glycerol, BSA
PTM	Unmodified
Clonality	Recombinant Monoclonal
Background	IL-9 is a cytokine secreted by CD4+ helper cells that acts as a regulator of a variety of hematopoietic cells. IL-9 stimulates cell proliferation and prevents apoptosis. It functions through the interleukin-9 receptor (IL9R), which activates different signal transducer and activator (STAT) proteins namely STAT1, STAT3 and STAT5. The gene encoding IL-9 has been identified as a candidate gene for asthma. Genetic studies on a mouse model of asthma demonstrated that IL-9 is a determining factor in the pathogenesis of bronchial hyperresponsiveness.
Cellular Localization	Secreted

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Menge: 100 ul

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Lieferung vsl. bis 19.02.2026

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