Anti-PPARGC1A Antibody

Primary Antibodies

91027 MW

PPARGC1A antibody can be used for detection of PPARGC1A by Western blot at 1 - 2 ?g/ml. Antibody can also be used for Immunohistochemistry starting at 5 ?g/mL. For immunofluorescence start at 20 ?g/mL.
Antibody validated: Western Blot in human and mouse samples; Immunohistochemistry in human samples and Immunofluorescence in human samples. All other applications and species not yet tested. Optimal dilutions for each application should be determined by the researcher.

Peroxisome proliferator-activated receptor gamma, coactivator 1 alpha

PPARGC1A antibody was raised against a 19 amino acid peptide near the carboxy terminus of human PPARGC1A. The immunogen is located within the last 50 amino acids of PPARGC1A.

PPARGC1A antibody is affinity chromatography purified via peptide column.

Obesity

Transcriptional coactivator for steroid receptors and
nuclear receptors. Greatly increases the transcriptional activity
of PPARG and thyroid hormone receptor on the uncoupling protein
promoter. Can regulate key mitochondrial genes that contribute to
the program of adaptive thermogenesis. Plays an essential role in
metabolic reprogramming in response to dietary availability
through coordination of the expression of a wide array of genes
involved in glucose and fatty acid metabolism. Induces the
expression of PERM1 in the skeletal muscle in an ESRRA-dependent
manner. Also involved in the integration of the circadian rhythms
and energy metabolism. Required for oscillatory expression of
clock genes, such as ARNTL/BMAL1 and NR1D1, through the
coactivation of RORA and RORC, and metabolic genes, such as PDK4
and PEPCK.

Boster Bio Anti-PPARGC1A Antibody (Catalog # A00236). Tested in ELISA, WB, IHC-P, IF applications. This antibody reacts with Human, Mouse, Rat.

Heart, skeletal muscle, liver and kidney.
Expressed at lower levels in brain and pancreas and at very low
levels in the intestine and white adipose tissue. In skeletal
muscle, levels were lower in obese than in lean subjects and
fasting induced a 2-fold increase in levels in the skeletal muscle
in obese subjects.