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research use only
Cat.No.: F4871
| Dilution |
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|
| Application |
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| WB, IHC, IF, FCM |
| Reactivity |
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| Mouse, Rat, Human |
| Source |
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| Rabbit Monoclonal Antibody |
| Storage Buffer |
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| PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3 |
| Storage (from the date of receipt) |
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| -20°C (avoid freeze-thaw cycles), 2 years |
| Predicted MW Observed MW |
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| 58 kDa 70 kDa |
| *Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. |
| Positive Control | Human spleen tissue; Mouse cardiac muscle tissue; Rat spleen tissue; Human thymus cells; Jurkat cells; Raji cells; Ramos cells |
|---|---|
| Negative Control |
| Specificity |
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| IKZF3 Antibody [D19G22] detects endogenous levels of total IKZF3 protein. |
| Clone |
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| D19G22 |
| Synonym(s) |
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| ZNFN1A3; IKZF3; Zinc finger protein Aiolos; Ikaros family zinc finger protein 3 |
| Background |
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| IKZF3 (Aiolos) is a hematopoietic-specific zinc finger transcription factor from the Ikaros family, essential for B-cell development and effector maturation. It contains an N-terminal DNA-binding domain with four tandem C2H2 zinc fingers that recognize the core GGAAA motif, particularly through major groove contacts made by key arginine and histidine residues, and a C-terminal dimerization domain with two additional zinc fingers that enable homo- and heterodimerization with other Ikaros proteins such as IKZF1 (Ikaros), IKZF2 (Helios), and IKZF4 (Eos), facilitating both repressive and activating transcriptional complexes. IKZF3 orchestrates sequential B-cell programming: initial IKZF1 homodimers establish lymphoid priming, while IKZF1:IKZF3 heterodimers recruit chromatin remodeling and co-repressor complexes such as NuRD, SWI/SNF, and PRC2 to silence pro-apoptotic genes and enforce survival checkpoints. As B cells mature, IKZF3 homodimers activate key regulators like BLIMP1, STAT3, and XBP1 to drive plasma cell differentiation and antibody secretion. In regulatory T cells, IKZF3 modulates IL-10 expression indirectly through synergy with FOXP3. Germline dominant-negative IKZF3 variants can interfere with IKZF1 function, repressing genes involved in B and T cell homing and leading to immunodeficiency, while somatic overexpression of IKZF3 sustains aberrant BCR and IL-7R signaling in leukemias. |
| References |
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