SHP_1, Human, Recombinant, E.coli
- Known as:
- SHP_1, Human, Recombinant, E.coli
- Catalog number:
- SHP2001
- Product Quantity:
- 0.5mg
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- SHP_1 Human Recombinant .coli
Related genes to: SHP_1, Human, Recombinant, E.coli
- Gene:
- CSHL1 NIH gene
- Name:
- chorionic somatomammotropin hormone like 1
- Previous symbol:
- CSHP1
- Synonyms:
- hCS-L, CSL, CS-5, MGC149868
- Chromosome:
- 17q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-01-12
- Gene:
- FCN2 NIH gene
- Name:
- ficolin 2
- Previous symbol:
- -
- Synonyms:
- P35, FCNL, EBP-37, ficolin-2
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-11
- Date modifiied:
- 2016-10-05
- Gene:
- PTPN6 NIH gene
- Name:
- protein tyrosine phosphatase non-receptor type 6
- Previous symbol:
- -
- Synonyms:
- HCP, HCPH, PTP-1C, SHP-1, SHP1
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-12
- Date modifiied:
- 2019-02-14
Related products to: SHP_1, Human, Recombinant, E.coli
Related articles to: SHP_1, Human, Recombinant, E.coli
- Signal regulatory protein alpha (SIRPα) is an inhibitory receptor expressed on macrophages and dendritic cells. Recent cancer research studies have reported evidence of upregulation of SIRPα on natural killer (NK) cells. The present study aimed to investigate the role of SIRPα in NK cells during viral infection. - Source: PubMed
Publication date: 2025/09/30
Cham Lamin BHamdan Thamer ABhat HilalTabbara Khaled SaeedFarid EmanBarbouche Mohamed RidhaAdomati Tom - Subarachnoid hemorrhage induces extensive neuronal cell death, leading to the release of damage-associated molecular patterns (DAMPs). These DAMPs, along with hemoglobin and cell corpses, trigger localized inflammation. Signal regulatory protein alpha (SIRPα) plays a crucial role in efferocytosis by acting as a "don't eat-me" signal, modulating inflammation and tissue homeostasis. However, the precise function and regulatory mechanisms of SIRPα in efferocytosis remain unclear. Proteomic analysis of cerebrospinal fluid (CSF) reveals that SIRPα levels are significantly elevated in the CSF of SAH patients and correlate with clinical outcomes. In vivo and in vitro studies show that microglial knockdown of SIRPα promotes efferocytosis and attenuates neuroinflammation following SAH. SIRPα inhibits efferocytosis by recruiting and phosphorylating SHP1 and SHP2 through phosphorylation of four tyrosine residues in its cytoplasmic domain, with SHP1 playing a particularly critical role. Mutation of these tyrosine residues to non-phosphorylatable alanine residues enhances efferocytosis and reduces neuroinflammation in vitro. RNA-seq analysis suggests that this mutation upregulates the expression of "eat-me" signals, MerTK and CD36, and identifies STAT6 as a key transcription factor involved in this process. In conclusion, SIRPα plays a central role in regulating microglia efferocytosis and neuroinflammation after SAH via the SHP1/STAT6 axis. Targeting this pathway may provide a promising therapeutic approach for SAH. - Source: PubMed
Publication date: 2025/03/19
Zhang BingtaoZou YanTang QikaiYuan ZixuanJiang KunZhang ZhaoxiangChen ShujuanWu QiZhou XiaomingZhang Xin - Shp1, encoded by the gene , is a protein tyrosine phosphatase that transduces inhibitory signals downstream of immunoreceptors in many immune cell types. Blocking Shp1 activity represents an exciting potential immunotherapeutic strategy for the treatment of cancer, as Shp1 inhibition would be predicted to unleash both innate and adaptive immunity against tumor cells. Antibodies blocking the interaction between CD47 on tumor cells and SIRPα on macrophages enhance macrophage phagocytosis, show efficacy in preclinical tumor models, and are being evaluated in the clinic. Here we found that Shp1 bound to phosphorylated peptide sequences derived from SIRPα and transduced the anti-phagocytic signal, as Shp1 loss in mouse bone marrow-derived macrophages increased phagocytosis of tumor cells . We also generated a novel mouse model to evaluate the impact of global, inducible deletion on anti-tumor immunity. We found that inducible Shp1 loss drove an inflammatory disease in mice that was phenotypically similar to that seen when is knocked out from birth. This indicates that acute perturbation of Shp1 could drive hyperactivation of immune cells, which could be therapeutically beneficial, though at the risk of potential toxicity. In this model, we found that Shp1 loss led to robust anti-tumor immunity against two immune-rich syngeneic tumor models that are moderately inflamed though not responsive to checkpoint inhibitors, MC38 and E0771. Shp1 loss did not promote anti-tumor activity in the non-inflamed B16F10 model. The observed activity in MC38 and E0771 tumors was likely due to effects of both innate and adaptive immune cells. Following Shp1 deletion, we observed increases in intratumoral myeloid cells in both models, which was more striking in E0771 tumors. E0771 tumors also contained an increased ratio of effector to regulatory T cells following Shp1 loss. This was not observed for MC38 tumors, though we did find increased levels of IFNγ, a cytokine produced by effector T cells, in these tumors. Overall, our preclinical data suggested that targeting Shp1 may be an attractive therapeutic strategy for boosting the immune response to cancer via a mechanism involving both innate and adaptive leukocytes. - Source: PubMed
Publication date: 2020/09/29
Myers Darienne RAbram Clare LWildes DavidBelwafa AmiraWelsh Alia M NSchulze Christopher JChoy Tiffany JNguyen TramOmaque NeilHu YongmeiSingh MallikaHansen RichGoldsmith Mark AQuintana ElsaSmith Jacqueline A MLowell Clifford A - Atherosclerosis is the process that underlies heart attack and stroke. A characteristic feature of the atherosclerotic plaque is the accumulation of apoptotic cells in the necrotic core. Prophagocytic antibody-based therapies are currently being explored to stimulate the phagocytic clearance of apoptotic cells; however, these therapies can cause off-target clearance of healthy tissues, which leads to toxicities such as anaemia. Here we developed a macrophage-specific nanotherapy based on single-walled carbon nanotubes loaded with a chemical inhibitor of the antiphagocytic CD47-SIRPα signalling axis. We demonstrate that these single-walled carbon nanotubes accumulate within the atherosclerotic plaque, reactivate lesional phagocytosis and reduce the plaque burden in atheroprone apolipoprotein-E-deficient mice without compromising safety, and thereby overcome a key translational barrier for this class of drugs. Single-cell RNA sequencing analysis reveals that prophagocytic single-walled carbon nanotubes decrease the expression of inflammatory genes linked to cytokine and chemokine pathways in lesional macrophages, which demonstrates the potential of 'Trojan horse' nanoparticles to prevent atherosclerotic cardiovascular disease. - Source: PubMed
Publication date: 2020/01/27
Flores Alyssa MHosseini-Nassab NiloufarJarr Kai-UweYe JianqinZhu XingjunWirka RobertKoh Ai LeenTsantilas PavlosWang YingNanda VivekKojima YokoZeng YitianLotfi MozhganSinclair RobertWeissman Irving LIngelsson ErikSmith Bryan RonainLeeper Nicholas J - Src homology 2 domain-containing protein tyrosine phosphatase substrate (SHPS)-1 is known to have regulatory effects on myeloid cells. However, its role in macrophage activation is not clearly understood. - Source: PubMed
Publication date: 2013/01/12
Kim Eun-JuSuk KyounghoLee Won-Ha