Bim Rabbit Polyclonal Antibody (CAB15771)
- SKU:
- CAB15771
- Product Type:
- Antibody
- Reactivity:
- Human
- Mouse
- Host Species:
- Rabbit
- Isotype:
- IgG
- Antibody Type:
- Polyclonal Antibody
- Research Area:
- Cell Death
Description
Product Name: | Bim Rabbit Polyclonal Antibody |
SKU: | CAB15771 |
Size: | 20uL, 100uL |
Isotype: | IgG |
Host Species: | Rabbit |
Reactivity: | Human,Mouse,Rat |
Immunogen: | A synthetic peptide corresponding to a sequence within amino acids 100-198 of human Bim (NP_619527.1). |
Sequence: | DTDR SPAP MSCD KSTQ TPSP PCQA FNHY LSAM ASMR QAEP ADMR PEIW IAQE LRRI GDEF NAYY ARRV FLNN YQAA EDHP RMVI LRLL RYIV RLVW RMH |
Tested Applications: | WB IF/ICC ELISA |
Recommended Dilution: | WB,1:500 - 1:1000 IF/ICC,1:50 - 1:200 |
Synonyms: | BAM; BIM; BOD; Bim |
Positive Sample: | 293T,MCF7,Raji,Mouse spleen |
Conjugate: | Unconjugated |
Cellular Localization: | Endomembrane system, Mitochondrion, Peripheral membrane protein. |
Calculated MW: | 22kDa |
Observed MW: | 18kDa/23kDa |
The protein encoded by this gene belongs to the BCL-2 protein family. BCL-2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. The protein encoded by this gene contains a Bcl-2 homology domain 3 (BH3). It has been shown to interact with other members of the BCL-2 protein family and to act as an apoptotic activator. The expression of this gene can be induced by nerve growth factor (NGF), as well as by the forkhead transcription factor FKHR-L1, which suggests a role of this gene in neuronal and lymphocyte apoptosis. Transgenic studies of the mouse counterpart suggested that this gene functions as an essential initiator of apoptosis in thymocyte-negative selection. Several alternatively spliced transcript variants of this gene have been identified.
Purification Method: | Affinity purification |
Gene ID: | 10018 |
Storage Buffer: | Store at -20℃. Avoid freeze / thaw cycles.Buffer: PBS with 0.05% proclin300,50% glycerol,pH7.3. |