CLCN7 Rabbit Polyclonal Antibody (CAB6886)
- SKU:
- CAB6886
- Product Type:
- Antibody
- Reactivity:
- Human
- Mouse
- Rat
- Host Species:
- Rabbit
- Isotype:
- IgG
- Antibody Type:
- Polyclonal Antibody
- Research Area:
- Signal Transduction
Frequently bought together:
Description
Product Name: | CLCN7 Rabbit Polyclonal Antibody |
SKU: | CAB6886 |
Size: | 20uL, 100uL |
Isotype: | IgG |
Host Species: | Rabbit |
Reactivity: | Human,Mouse,Rat |
Immunogen: | Recombinant fusion protein containing a sequence corresponding to amino acids 626-805 of human CLCN7 (NP_001278.1). |
Sequence: | TARE VMST PVTC LRRR EKVG VIVD VLSD TASN HNGF PVVE HADD TQPA RLQG LILR SQLI VLLK HKVF VERS NLGL VQRR LRLK DFRD AYPR FPPI QSIH VSQD EREC TMDL SEFM NPSP YTVP QEAS LPRV FKLF RALG LRHL VVVD NRNQ VVGL VTRK DLAR YRLG KRGL EELS LAQT |
Tested Applications: | WB ELISA |
Recommended Dilution: | WB,1:500 - 1:2000 |
Synonyms: | HOD; CLC7; CLC-7; OPTA2; OPTB4; PPP1R63; CLCN7 |
Positive Sample: | SK-OV-3 |
Conjugate: | Unconjugated |
Cellular Localization: | Lysosome membrane, Multi-pass membrane protein. |
Calculated MW: | 89kDa |
Observed MW: | 110kDa |
The product of this gene belongs to the CLC chloride channel family of proteins. Chloride channels play important roles in the plasma membrane and in intracellular organelles. This gene encodes chloride channel 7. Defects in this gene are the cause of osteopetrosis autosomal recessive type 4 (OPTB4), also called infantile malignant osteopetrosis type 2 as well as the cause of autosomal dominant osteopetrosis type 2 (OPTA2), also called autosomal dominant Albers-Schonberg disease or marble disease autosoml dominant. Osteopetrosis is a rare genetic disease characterized by abnormally dense bone, due to defective resorption of immature bone. OPTA2 is the most common form of osteopetrosis, occurring in adolescence or adulthood.
Purification Method: | Affinity purification |
Gene ID: | 1186 |
Storage Buffer: | Store at -20℃. Avoid freeze / thaw cycles.Buffer: PBS with 0.02% sodium azide,50% glycerol,pH7.3. |