Human Recombinant HSPB1
Reference ID:KB-2236
Western Blot
Gene of Interest
Gene Synonyms:HSPB1;HSP27;HSP28
Protein Names:Heat shock protein beta-1 (HspB1) (28 kDa heat shock protein) (Estrogen-regulated 24 kDa protein) (Heat shock 27 kDa protein) (HSP 27) (Stress-responsive protein 27) (SRP27)
Accession Data
Organism:Homo sapiens (Human)
Mass (kDa):227.83
Length (aa):205
Proteomics (Proteome ID):UP000005640
Proteomics (Chromosome): Chromosome 7
Function [CC]:Small heat shock protein which functions as a molecular chaperone probably maintaining denatured proteins in a folding-competent state (PubMed:10383393, PubMed:20178975). Plays a role in stress resistance and actin organization (PubMed:19166925). Through its molecular chaperone activity may regulate numerous biological processes including the phosphorylation and the axonal transport of neurofilament proteins (PubMed:23728742). {ECO:0000269|PubMed:10383393, ECO:0000269|PubMed:19166925, ECO:0000269|PubMed:20178975, ECO:0000269|PubMed:23728742}.
Induction:Up-regulated in response to environmental stresses such as heat shock (PubMed:8325890). Up-regulated by estrogen stimulation (PubMed:2743305). {ECO:0000269|PubMed:2743305, ECO:0000269|PubMed:8325890}.; (Microbial infection) Up-regulated in response to enterovirus 71 (EV71) infection (at protein level). {ECO:0000269|PubMed:16548883}.
Tissue Specificity:Detected in all tissues tested: skeletal muscle, heart, aorta, large intestine, small intestine, stomach, esophagus, bladder, adrenal gland, thyroid, pancreas, testis, adipose tissue, kidney, liver, spleen, cerebral cortex, blood serum and cerebrospinal fluid. Highest levels are found in the heart and in tissues composed of striated and smooth muscle. {ECO:0000269|PubMed:1560006}.
Disease:Charcot-Marie-Tooth disease 2F (CMT2F) [MIM:606595]: A dominant axonal form of Charcot-Marie-Tooth disease, a disorder of the peripheral nervous system, characterized by progressive weakness and atrophy, initially of the peroneal muscles and later of the distal muscles of the arms. Charcot-Marie-Tooth disease is classified in two main groups on the basis of electrophysiologic properties and histopathology: primary peripheral demyelinating neuropathies (designated CMT1 when they are dominantly inherited) and primary peripheral axonal neuropathies (CMT2). Neuropathies of the CMT2 group are characterized by signs of axonal degeneration in the absence of obvious myelin alterations, normal or slightly reduced nerve conduction velocities, and progressive distal muscle weakness and atrophy. Onset of Charcot-Marie-Tooth disease type 2F is between 15 and 25 years with muscle weakness and atrophy usually beginning in feet and legs (peroneal distribution). Upper limb involvement occurs later. {ECO:0000269|PubMed:15122254, ECO:0000269|PubMed:20178975, ECO:0000269|PubMed:22176143, ECO:0000269|PubMed:22206013, ECO:0000269|PubMed:23728742}. Note=The disease is caused by mutations affecting the gene represented in this entry.; Neuronopathy, distal hereditary motor, 2B (HMN2B) [MIM:608634]: A neuromuscular disorder. Distal hereditary motor neuronopathies constitute a heterogeneous group of neuromuscular disorders caused by selective degeneration of motor neurons in the anterior horn of the spinal cord, without sensory deficit in the posterior horn. The overall clinical picture consists of a classical distal muscular atrophy syndrome in the legs without clinical sensory loss. The disease starts with weakness and wasting of distal muscles of the anterior tibial and peroneal compartments of the legs. Later on, weakness and atrophy may expand to the proximal muscles of the lower limbs and/or to the distal upper limbs. {ECO:0000269|PubMed:15122254, ECO:0000269|PubMed:18832141, ECO:0000269|PubMed:18952241, ECO:0000269|PubMed:20178975, ECO:0000269|PubMed:20870250, ECO:0000269|PubMed:22176143, ECO:0000269|PubMed:23643870, ECO:0000269|PubMed:23728742, ECO:0000269|PubMed:23948568, ECO:0000269|PubMed:25965061, ECO:0000269|PubMed:28144995}. Note=The disease is caused by mutations affecting the gene represented in this entry.
Mutagenesis:MUTAGEN 15 15 S->D: Mimicks phosphorylation state, leading to dreased ability to act as molecular chaperones; when associated with D-78 and D-82. {ECO:0000269|PubMed:10383393}.; MUTAGEN 78 78 S->D: Mimicks phosphorylation state, leading to dreased ability to act as molecular chaperones; when associated with D-15 and D-82. {ECO:0000269|PubMed:10383393}.; MUTAGEN 82 82 S->D: Mimicks phosphorylation state, leading to dreased ability to act as molecular chaperones; when associated with D-15 and D-78. {ECO:0000269|PubMed:10383393}.
Reagent Data
Class:Heat Shock
Molecular Weight:22.7
Formulation:Sterile-filtered colorless solution
Formulation Concentration:1 mg/ml
Buffer Volume:20 mM
Buffer Solution: HEPES
KCl:100 mM
Reducing Agents
DTT:1 mM
Purity:> 95%
Determined: SDS-PAGE
Sample Handling
Stability:This bioreagent is stable at 4°C (short-term) and -70°C(long-term). After reconstitution, sample may be stored at 4°C for 2-7 days and below -18°C for future use.
Preparation:Reconstitute in sterile distilled H2O to no less than 100 ug/ml; dilute reconstituted stock further in other aqueous solutions if needed. Please review COA for lot-specific instructions. Final measurements should be determined by the end-user for optimal performance.