Anti-Placental Lactogen / CSH1 antibody

Anti-Placental Lactogen / CSH1 antibody

• DataSheet
• Material Safety Data Sheets (MSDS)

Rabbit polyclonal to Placental Lactogen / CSH1

ELISA, IHC-P

Mouse Acetylcholinesterase / ACHE

lactogen antibody; CS-1 antibody; CSA antibody; PL antibody; Placental Lactogen antibody; PL antibody; CSA antibody; CS-1 antibody; CSMT antibody; hCS-1 antibody; hCS-A antibody; Pl1 antibody; Csh1 antibody; PL-I antibody; Pl-1 antibody; PL-Ia antibody; mPL-I antibody; AI325057 antibody; PL-I-alpha antibody; CSH1 antibody; CSH2 antibody; CSMT antibody; FLJ75407 antibody; hCS-A antibody

Rabbit IgG

Produced in rabbits immunized with purified, recombinant Mouse Acetylcholinesterase / ACHE (rM Acetylcholinesterase / ACHE; NP_033729.1; Met 1-Leu 614). Acetylcholinesterase / ACHE specific IgG was purified by Mouse Acetylcholinesterase / ACHE affinity chromatography.

Polyclonal

0.2 μm filtered solution in PBS with 5% trehalose

This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free.
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.

Chorionic somatomammotropin hormone, also known as Choriomammotropin, Lactogen, Placental lactogen and CSH1, is a secreted protein which belongs to the somatotropin / prolactin family. CSH1 is produced only during pregnancy and is involved in stimulating lactation, fetal growth and metabolism. Does not interact with GHR but only activates PRLR through zinc-induced dimerization. The CSH1 gene is member of the GH gene cluster on 17q, which consists of two growth hormone genes and three CSH genes. Genomic alterations in the GH cluster are well known, causing different phenotypes depending on the size of the deletion and the genes involved. The increased prevalence of hemizygosity of CSH1 in population in comparison to controls indicates a role for CSH1 haploinsufficiency in the etiology of growth retardation. Investigation of CSH1 deletions in further SRS and growth retarded patients will enable us to establish under which circumstances haploinsufficiency of CSH1 is likely to result in clinical changes.

• Prager,S. et al., 2003,Genet Test. 7 (3):259-63.
• Singleton, DR. et al., 2004, Microbiology. 150 (Pt 2): 285-92.
• Chen,Y. et al., 2008, Cancer Res. 68 (23):9729-34.