The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Use a concentration of 1 µg/ml. Detects a band of approximately 65 kDa (predicted molecular weight: 65 kDa).
Catalyzes the methylthiolation of N6-threonylcarbamoyladenosine (t(6)A), leading to the formation of 2-methylthio-N6-threonylcarbamoyladenosine (ms(2)t(6)A) at position 37 in tRNAs that read codons beginning with adenine.
Expressed in pancreatic islets.
Involvement in disease
Genetic variations in CDKAL1 are a cause of susceptibility to diabetes mellitus, non-insulin-dependent (NIDDM) [MIM:125853]. A multifactorial disorder of glucose homeostasis caused by a lack of sensitivity to the body's own insulin. Affected individuals usually have an obese body habitus and manifestations of a metabolic syndrome characterized by diabetes, insulin resistance, hypertension and hypertriglyceridemia. The disease results in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.
Belongs to the methylthiotransferase family. CDKAL1 subfamily. Contains 1 MTTase N-terminal domain. Contains 1 TRAM domain.
Endoplasmic reticulum membrane. Is a tail-anchored protein that exploits the TCR40 pathway for insertion into the endoplasmic reticulum.
This blot was produced using a 4-12% Bis-tris gel under the MOPS buffer system. The gel was run at 200V for 50 minutes before being transferred onto a Nitrocellulose membrane at 30V for 70 minutes. The membrane was then blocked for an hour using 2% Bovine Serum Albumin before being incubated with ab68045 overnight at 4°C. Antibody binding was detected using an anti-rabbit antibody conjugated to HRP, and visualised using ECL development solution ab133406.
Western blot - CDKAL1 antibody (ab68045)
All lanes : Anti-CDKAL1 antibody (ab68045) at 1 µg/ml
Palmer CJ et al. Cdkal1, a type 2 diabetes susceptibility gene, regulates mitochondrial function in adipose tissue. Mol Metab6:1212-1225 (2017).
Read more (PubMed: 29031721) »
Okamura T et al. Deletion of CDKAL1 affects high-fat diet-induced fat accumulation and glucose-stimulated insulin secretion in mice, indicating relevance to diabetes. PLoS One7:e49055 (2012).
Read more (PubMed: 23173044) »