Thermo Fisher Scientific SP110 Monoclonal Antibody (OTI4C1)
SP110 단백질을 인식하는 Mouse IgG1 단일클론 항체로, Western blot 및 IHC(P) 분석에 적합합니다. 인간 반응성으로, 액상 형태이며 1 mg/mL 농도로 제공됩니다. PBS/BSA/glycerol 버퍼에 보존되며 연구용으로만 사용됩니다.
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Applications
Western Blot (WB)
- Tested Dilution: 1:2,000
Immunohistochemistry (Paraffin) (IHC (P))
- Tested Dilution: 1:150
Product Specifications
| 항목 | 내용 |
|---|---|
| Species Reactivity | Human |
| Host / Isotype | Mouse / IgG1 |
| Class | Monoclonal |
| Type | Antibody |
| Clone | OTI4C1 |
| Immunogen | Human recombinant protein fragment corresponding to amino acids 232–521 of SP110 produced in E. coli |
| Conjugate | Unconjugated |
| Form | Liquid |
| Concentration | 1 mg/mL |
| Purification | Affinity Chromatography |
| Storage Buffer | PBS, pH 7.3, with 1% BSA, 50% glycerol |
| Contains | 0.02% sodium azide |
| Storage Conditions | -20°C, Avoid Freeze/Thaw Cycles |
| Shipping Conditions | Ambient (domestic); Wet ice (international) |
| RRID | AB_2725400 |
Target Information
Susceptibility to tuberculosis (TB) in mice has recently been attributed to the IPR1 gene. IPR1 is a member of the SP100/SP140 family of nuclear body proteins and encodes a leukocyte-specific nuclear body component. The protein functions as an activator of gene transcription and may serve as a nuclear hormone receptor coactivator.
Alternative splicing has been observed for this gene, and three transcript variants encoding distinct isoforms have been identified. SP110 is the closest homolog of the IPR1 protein in humans. The IPR1/SP110 gene product may play a role in integrating signals generated by intracellular pathogens with mechanisms controlling innate immunity, cell death, and pathogenesis.
IPR1/SP110 is up-regulated after infection with M. tuberculosis and required by Anaplasma phagocytophilum for infection of human promyelocytic cells. Defects in SP110 are associated with impaired resistance to M. tuberculosis infection.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
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