bs-9327R [Primary Antibody]
LRCH1 Polyclonal Antibody
www.biossusa.com
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Host: Rabbit

Target Protein: LRCH1

Immunogen Range: 221-320/728


Clonality: Polyclonal

Isotype: IgG

Entrez Gene: 23143

Swiss Prot: Q9Y2L9

Source: KLH conjugated synthetic peptide derived from human LRCH1

Purification: Purified by Protein A.

Storage Buffer: 0.01M TBS(pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.

Storage: Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.

Background:

Members of the leucine-rich repeat family include LRCH1, LRCH2, LRCH3 and LRCH4. All family members contain one calponin-homology domain and nine leucine-rich repeats. The gene encoding LRCH1, also known as Neuronal protein 81 (NP81), has been suggested to be a possible gene locus for susceptibility to osetoarthritis, especially in women, though studies have shown conflicting results. LRCH1 is a 728 amino acid protein that is expressed at highest levels in cerebellum, with lower levels of expression in spinal cord, ovary, kidney and amygdala. In pigs, the gene encoding LRCH1 is one of 22 genes that is associated with leg and body conformation traits that affect productivity and health. There are two isoforms of LRCH1 that are expressed as a result of alternative splicing events.

Size: 100ul

Concentration: 1ug/ul

Applications: IHC(1:100-500)

Predicted Molecular Weight: 81


Cross Reactive Species: Human
Mouse
Rat

Predicted Cross Reactive Species: Cow
Sheep
Pig
Horse
Chicken
Rabbit

For research use only. Not intended for diagnostic or therapeutic use.

PRODUCT SPECIFIC PUBLICATIONS
  • Chen WK et al. Leucine rich repeats and calponin homology domain containing 1 inhibits microglia-mediated neuroinflammation in a rat traumatic spinal cord injury model. Journal of Neuroinflammation.2019.Read more>>
  • Wen-Kai Chenet al. Inhibition of leucine-rich repeats and calponin homology domain containing 1 accelerates microglia-mediated neuroinflammation in a rat traumatic spinal cord injury model. J Neuroinflammation. 2020 Jul 6;17(1):202.Read more>>