This antibody detects an 25 kDa protein, corresponding to the apparent molecular mass of Heat Shock Protein 27 (Hsp27) on SDS-PAGE immunoblots. This antibody has been shown to react with both the phosphorylated and the non-phosphorylated forms of Hsp27. Note: It has been reported that certain murine cell lines do not express Hsp27 under certain conditions. This antibody also recognizes a mitochondrial small Hsp (35 kDa) in rat PC12 cells. This mitochondrial small Hsp is proposed to protect mitochondrial complex I from oxidative stress.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Use a concentration of 10 µg/ml.
Use at an assay dependent concentration.
1/1 - 1/1000. Predicted molecular weight: 25 kDa.
1/1 - 1/100.
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 (ab12351)
All lanes : Anti-Hsp27 antibody (ab12351) at 1 µg/ml
Lane 1 : MW Marker Lane 2 : HSP27 Recombinant Human Protein Lane 3 : HSP25 Recombinant Murine Protein (Negative Control) Lane 4 : HeLa cell lysate Lane 5 : HeLa cell lysate, Heat Shocked Lane 6 : Vero, Heat Shocked Lane 7 : 3T3 cell lysate, heat shocked Lane 8 : PC-12 cell lysate, Heat Shocked
Bauer AJ et al. Pravastatin attenuates hypertension, oxidative stress, and angiogenic imbalance in rat model of placental ischemia-induced hypertension. Hypertension61:1103-10 (2013).
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