All HSP60 reagents are produced in house and quality controlled, including 4 HSP60 Antibody, 45 HSP60 Gene, 3 HSP60 IPKit, 2 HSP60 Protein, 3 HSP60 qPCR. All HSP60 reagents are ready to use.
Recombinant HSP60 proteins are expressed by E. coli with fusion tags as N-GST & His, N-His.
HSP60antibodies are validated with different applications, which are IHC-P, WB, IP, ELISA, ICC/IF, IF.
HSP60cDNA clones are full length sequence confirmed and expression validated. There are 13 kinds of tags for each HSP60 of different species, especially GFP tag, OFP tag, FLAG tag and so on. There are three kinds of vectors for choice, cloning vector, expression vector and lentivrial expression vector.
HSPD1, also known as HSP60, is a member of the chaperonin family. HSPD1 may function as a signaling molecule in the innate immune system. This protein is essential for the folding and assembly of newly imported proteins in the mitochondria. It may also prevent misfolding and promote the refolding and proper assembly of unfolded polypeptides generated under stress conditions in the mitochondrial matrix. HSPD1 gene is adjacent to a related family member and the region between the 2 genes functions as a bidirectional promoter. Several pseudogenes have been associated with this gene. Mutations associated with this gene cause autosomal recessive spastic paraplegia 13.Defects in HSPD1 are a cause of spastic paraplegia autosomal dominant type 13 (SPG13). Spastic paraplegia is a degenerative spinal cord disorder characterized by a slow, gradual, progressive weakness and spasticity of the lower limbs. Defects in HSPD1 are the cause of leukodystrophy hypomyelinating type 4 (HLD4); also called mitochondrial HSP60 chaperonopathy or MitCHAP-60 disease. HLD4 is a severe autosomal recessive hypomyelinating leukodystrophy. HSPD1 is cinically characterized by infantile-onset rotary nystagmus, progressive spastic paraplegia, neurologic regression, motor impairment, profound mental retardation. Death usually occurrs within the first two decades of life.