Immunohistochemistry with formalin fixed paraffin embedded tissues: 4 μg/mL Antigen retrieval: Steam slides in 0.01 M sodium citrate buffer, pH 6.0, at 99-100 °C for 20 min. Remove from heat and let stand at room temperature in buffer for 20 min. Rinse in 1x TBS with Tween (TBST) for 1 min. at room temperature. Other applications not tested. Optimal dilutions are dependent on conditions and should be determined by the user. Further Comments: This product was originally produced by MBL International.
限制
仅限研究用
浓度
1.0 mg/mL
缓冲液
PBS containing 0.09 % Sodium Azide as preservative
储存液
Sodium azide
注意事项
This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
储存条件
4 °C/-80 °C
储存方法
Store the antibody undiluted at 2-8 °C for one month or (in aliquots) at -70 °C for longer. Avoid repeated freezing and thawing. Shelf life: one year from despatch.
有效期
12 months
抗原
NR0B2
(Nuclear Receptor Subfamily 0, Group B, Member 2 (NR0B2))
SHP antibody, SHP1 antibody, SHP-1 antibody, Shp1 antibody, Shp antibody, NR0B2-A antibody, Nr0b2 antibody, SHP-A antibody, gb:bc058069 antibody, nuclear receptor subfamily 0 group B member 2 antibody, nuclear receptor subfamily 0, group B, member 2 antibody, nuclear receptor subfamily 0, group B, member 2a antibody, NR0B2 antibody, Nr0b2 antibody, nr0b2a antibody
背景
SHP (short heterodimer partner) is a bile acid-dependent orphan NR0 Knirps-Like receptor with dimerization and ligand-binding domains but not the conventional DNA-binding domain. SHP has been shown to inhibit the transcriptional activity of other nuclear receptors, including thyroid hormone receptor, constitutive androstane receptor, and retinoic acid receptors. SHP affects hepatic cholesterol catabolism based on a two-step mechanism dependent on both coactivator competition and direct transcriptional repression by mediating the repression of CYP7A1, the rate-limiting enzyme for bile acid synthesis. Mutations in the SHP gene contribute to increased body weight, indicating a possible role of SHP in the development of early-onset diabetes (maturity-onset diabetes of the young, MODY). Loss of SHP in mice caused abnormal accumulation and increased synthesis of bile acids due to derepression of rate-limiting CYP7A1 and CYP8B1 hydroxylase enzymes in the biosynthetic pathway. SHP expression has been documented in human liver, adrenal, spleen, and pancreas. ESTs have been isolated from cancerous human kidney, lung, and stomach, as well as normal human heart, kidney, liver, and liver/spleen. Caution: The nuclear receptor SHP should not be confused with the tyrosine phosphatases SHP-1 and SHP-2.Synonyms: Nuclear receptor subfamily 0 group B member 2, Orphan nuclear receptor SHP, SHP, Small heterodimer partner