The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
1/500 - 1/2000. Detects a band of approximately 23 kDa (predicted molecular weight: 23 kDa).
1/100 - 1/250. Perform heat mediated antigen retrieval before commencing with IHC staining protocol.
1/50 - 1/100.
Is unsuitable for Flow Cyt or IP.
Involved in stress resistance and actin organization.
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.
Involvement in disease
Defects in HSPB1 are the cause of Charcot-Marie-Tooth disease type 2F (CMT2F) [MIM:606595]. CMT2F is a form of Charcot-Marie-Tooth disease, the most common inherited disorder of the peripheral nervous system. Charcot-Marie-Tooth disease is classified in two main groups on the basis of electrophysiologic properties and histopathology: primary peripheral demyelinating neuropathy or CMT1, and primary peripheral axonal neuropathy or CMT2. Neuropathies of the CMT2 group are characterized by signs of axonal regeneration in the absence of obvious myelin alterations, normal or slightly reduced nerve conduction velocities, and progressive distal muscle weakness and atrophy. Nerve conduction velocities are normal or slightly reduced. CMT2F onset is between 15 and 25 years with muscle weakness and atrophy usually beginning in feet and legs (peroneal distribution). Upper limb involvement occurs later. CMT2F inheritance is autosomal dominant. Defects in HSPB1 are a cause of distal hereditary motor neuronopathy type 2B (HMN2B) [MIM:608634]. Distal hereditary motor neuronopathies constitute a heterogeneous group of neuromuscular disorders caused by selective impairment 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.
Belongs to the small heat shock protein (HSP20) family.
Phosphorylated in MCF-7 cells on exposure to protein kinase C activators and heat shock.
Cytoplasm. Nucleus. Cytoplasm > cytoskeleton > spindle. Cytoplasmic in interphase cells. Colocalizes with mitotic spindles in mitotic cells. Translocates to the nucleus during heat shock and resides in sub-nuclear structures known as SC35 speckles or nuclear splicing speckles.
heat shock protein family B (small) member 1 antibody
Hsp 25 antibody
HSP 27 antibody
Hsp 28 antibody
Hsp B1 antibody
Stress responsive protein 27 antibody
Stress-responsive protein 27 antibody
Western blot - Anti-Hsp27 antibody [EP1724Y] (ab62339)
Lane 1: Wild type HAP1 whole cell lysate (20 µg) Lane 2: Hsp27 knockout HAP1 whole cell lysate (20 µg) Lane 3: HeLa whole cell lysate (20 µg) Lane 4: MCF7 whole cell lysate (20 µg)
Lanes 1 - 4: Merged signal (red and green). Green - ab62339 observed at 27 kDa. Red - loading control, ab8245, observed at 37 kDa.
ab62339 was shown to specifically react with Hsp27 in wild-type HAP1 cells. No band was observed when Hsp27 knockout samples were used. Wild-type and Hsp27 knockout samples were subjected to SDS-PAGE. Ab62339 and ab8245 (Mouse anti GAPDH loading control) were incubated overnight at 4°C at 500 dilution and 1/20000 dilution respectively. Blots were developed with Goat anti-Rabbit IgG H&L (IRDye® 800CW) preabsorbed ab216773 and Goat anti-Mouse IgG H&L (IRDye® 680RD) preabsorbed ab216776 secondary antibodies at 1/20000 dilution for 1 hour at room temperature before imaging.
Booth L et al. PDE5 inhibitors enhance the lethality of pemetrexed through inhibition of multiple chaperone proteins and via the actions of cyclic GMP and nitric oxide. Oncotarget8:1449-1468 (2017).
Read more (PubMed: 27903966) »
Booth L et al. The HDAC inhibitor AR42 interacts with pazopanib to kill trametinib/dabrafenib-resistant melanoma cells in vitro and in vivo. Oncotarget8:16367-16386 (2017).
Read more (PubMed: 28146421) »