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Rabbit Anti-INPP5D Recombinant Antibody (CBXS-5997) (CBMAB-S0843-CQ)

This product is a rabbit antibody that recognizes INPP5D. The antibody CBXS-5997 can be used for immunoassay techniques such as: WB, IP, IF, FC.
See all INPP5D antibodies

Summary

Host Animal
Rabbit
Specificity
Human
Clone
CBXS-5997
Application
WB, IP, IF, FC

Basic Information

Specificity
Human
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Inositol Polyphosphate-5-Phosphatase D
Introduction
This gene is a member of the inositol polyphosphate-5-phosphatase (INPP5) family and encodes a protein with an N-terminal SH2 domain, an inositol phosphatase domain, and two C-terminal protein interaction domains. Expression of this protein is restricted to hematopoietic cells where its movement from the cytosol to the plasma membrane is mediated by tyrosine phosphorylation. At the plasma membrane, the protein hydrolyzes the 5' phosphate from phosphatidylinositol (3,4,5)-trisphosphate and inositol-1,3,4,5-tetrakisphosphate, thereby affecting multiple signaling pathways. The protein is also partly localized to the nucleus, where it may be involved in nuclear inositol phosphate signaling processes. Overall, the protein functions as a negative regulator of myeloid cell proliferation and survival. Mutations in this gene are associated with defects and cancers of the immune system. Alternative splicing of this gene results in multiple transcript variants.
Entrez Gene ID
3635
UniProt ID
Q92835
Alternative Names
Inositol Polyphosphate-5-Phosphatase D
Function
Phosphatidylinositol (PtdIns) phosphatase that specifically hydrolyzes the 5-phosphate of phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P3) to produce PtdIns(3,4)P2, thereby negatively regulating the PI3K (phosphoinositide 3-kinase) pathways (PubMed:8723348, PubMed:10764818, PubMed:8769125).
Able also to hydrolyzes the 5-phosphate of phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P3) and inositol 1,3,4,5-tetrakisphosphate (PubMed:9108392, PubMed:10764818, PubMed:8769125).
Acts as a negative regulator of B-cell antigen receptor signaling. Mediates signaling from the FC-gamma-RIIB receptor (FCGR2B), playing a central role in terminating signal transduction from activating immune/hematopoietic cell receptor systems. Acts as a negative regulator of myeloid cell proliferation/survival and chemotaxis, mast cell degranulation, immune cells homeostasis, integrin alpha-IIb/beta-3 signaling in platelets and JNK signaling in B-cells. Regulates proliferation of osteoclast precursors, macrophage programming, phagocytosis and activation and is required for endotoxin tolerance. Involved in the control of cell-cell junctions, CD32a signaling in neutrophils and modulation of EGF-induced phospholipase C activity (PubMed:16682172).
Key regulator of neutrophil migration, by governing the formation of the leading edge and polarization required for chemotaxis. Modulates FCGR3/CD16-mediated cytotoxicity in NK cells. Mediates the activin/TGF-beta-induced apoptosis through its Smad-dependent expression.
Biological Process
Apoptotic processIEA:UniProtKB-KW
Determination of adult lifespanIEA:Ensembl
Immunoglobulin mediated immune responseIEA:Ensembl
Intracellular signal transductionIEA:Ensembl
Negative regulation of B cell proliferationIEA:Ensembl
Negative regulation of bone resorptionIEA:Ensembl
Negative regulation of immune responseIEA:Ensembl
Negative regulation of interleukin-6 productionIEA:Ensembl
Negative regulation of monocyte differentiationIEA:Ensembl
Negative regulation of neutrophil differentiationIEA:Ensembl
Negative regulation of osteoclast differentiationIEA:Ensembl
Negative regulation of signal transductionIEA:Ensembl
Phosphate-containing compound metabolic processManual Assertion Based On ExperimentTAS:ProtInc
Phosphatidylinositol biosynthetic processTAS:Reactome
Phosphatidylinositol dephosphorylationIEA:InterPro
Positive regulation of apoptotic processIEA:Ensembl
Positive regulation of B cell differentiationIEA:Ensembl
Positive regulation of erythrocyte differentiationIEA:Ensembl
Signal transductionManual Assertion Based On ExperimentTAS:ProtInc
T cell receptor signaling pathwayTAS:Reactome
Cellular Location
Cytoplasm; Cell membrane; Membrane raft; Cytoplasm, cytoskeleton; Membrane. Translocates to the plasma membrane when activated, translocation is probably due to different mechanisms depending on the stimulus and cell type. Translocates from the cytoplasm to membrane ruffles in a FCGR3/CD16-dependent manner. Colocalizes with FC-gamma-RIIB receptor (FCGR2B) or FCGR3/CD16 at membrane ruffles. Tyrosine phosphorylation may also participate in membrane localization.
PTM
Tyrosine phosphorylated by the members of the SRC family after exposure to a diverse array of extracellular stimuli such as cytokines, growth factors, antibodies, chemokines, integrin ligands and hypertonic and oxidative stress. Phosphorylated upon IgG receptor FCGR2B-binding.

Castranio, E. L., Hasel, P., Haure‐Mirande, J. V., Ramirez Jimenez, A. V., Hamilton, B. W., Kim, R. D., ... & Ehrlich, M. E. (2023). Microglial INPP5D limits plaque formation and glial reactivity in the PSAPP mouse model of Alzheimer's disease. Alzheimer's & Dementia, 19(6), 2239-2252.

Olufunmilayo, E. O., & Holsinger, R. D. (2023). INPP5D/SHIP1: Expression, Regulation and Roles in Alzheimer’s Disease Pathophysiology. Genes, 14(10), 1845.

Lin, P. B. C., Tsai, A. P. Y., Soni, D., Lee‐Gosselin, A., Moutinho, M., Puntambekar, S. S., ... & Oblak, A. L. (2023). INPP5D deficiency attenuates amyloid pathology in a mouse model of Alzheimer's disease. Alzheimer's & Dementia, 19(6), 2528-2537.

Luan, W., Sun, Z., Wu, C., Tao, M., & Shen, X. (2023). Neuroinflammation after ischemic stroke involves INPP5D expression mediated by the TMPO-AS1-PU. 1 complex. Neurological Research, 45(4), 319-333.

Gandy, S., & Ehrlich, M. E. (2023). miR155, TREM2, INPP5D: Disease stage and cell type are essential considerations when targeting clinical interventions based on mouse models of Alzheimer’s amyloidopathy. Journal of Neuroinflammation, 20(1), 1-5.

Zajac, D. J., Simpson, J., Zhang, E., Parikh, I., & Estus, S. (2023). Expression of INPP5D Isoforms in Human Brain: Impact of Alzheimer’s Disease Neuropathology and Genetics. Genes, 14(3), 763.

Iguchi, A., Takatori, S., Kimura, S., Muneto, H., Wang, K., Etani, H., ... & Tomita, T. (2023). INPP5D modulates TREM2 loss-of-function phenotypes in a β-amyloidosis mouse model. Iscience, 26(4).

Tsai, A. P., Lin, P. B. C., Dong, C., Moutinho, M., Casali, B. T., Liu, Y., ... & Nho, K. (2021). INPP5D expression is associated with risk for Alzheimer's disease and induced by plaque-associated microglia. Neurobiology of disease, 153, 105303.

Yao, X., Risacher, S. L., Nho, K., Saykin, A. J., Wang, Z., Shen, L., & Alzheimer's Disease Neuroimaging Initiative. (2019). Targeted genetic analysis of cerebral blood flow imaging phenotypes implicates the INPP5D gene. Neurobiology of aging, 81, 213-221.

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For research use only. Not intended for any clinical use.

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