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SH2B1 encodes a member of the SH2-domain containing mediators family. Additionally we are shipping SH2B Adaptor Protein 1 Proteins (6) and many more products for this protein.
Showing 10 out of 62 products:
Human Monoclonal SH2B1 Primary Antibody for IF, WB - ABIN968576
Rothenberg: Bioethics commission to review gene patenting. in Bio/technology (Nature Publishing Company) 1998
Show all 7 references for ABIN968576
Human Polyclonal SH2B1 Primary Antibody for EIA, WB - ABIN954785
Holzapfel, Grallert, Huth, Wahl, Fischer, Döring, Rückert, Hinney, Hebebrand, Wichmann, Hauner, Illig, Heid: Genes and lifestyle factors in obesity: results from 12,462 subjects from MONICA/KORA. in International journal of obesity (2005) 2010
Show all 2 references for ABIN954785
Dog (Canine) Polyclonal SH2B1 Primary Antibody for IHC, WB - ABIN2786119
Donatello, Fiorino, DeglInnocenti, Alberti, Miranda, Gorla, Bongarzone, Rizzetti, Pierotti, Borrello: SH2B1beta adaptor is a key enhancer of RET tyrosine kinase signaling. in Oncogene 2007
Human Polyclonal SH2B1 Primary Antibody for ELISA, WB - ABIN184601
OBrien, OShea, Carter-Su: SH2-B family members differentially regulate JAK family tyrosine kinases. in The Journal of biological chemistry 2002
that SH2B1 is a key positive mediator of pathological cardiac hypertrophy
Mutation analysis has demonstrated that variation in the SH2B1 gene is frequent in both lean and obese groups, with distinctive variations being present on either side of the weight spectrum.
The rs7359397 (SH2B1) was associated with the body weight, body mass index, and truncal fat mass reduction.
4 novel variants in SH2B1 were identified in individuals with obesity and insulin (show INS Antibodies) resistance.
This study highlighted the importance of two candidate genes, SH2B1 and FAIM2 (show FAIM2 Antibodies), in the risk of overweight/obesity.
SH2B1 can enhance neurite outgrowth and accelerate the maturation of human induced neurons under defined conditions.
Data (from in excess (show RCC1 Antibodies) of six genetic association studies) suggest that an SNP in SH2B1 (rs4788102) is not associated with abnormal glucose homeostasis in obese subjects of European ancestry. [META-ANALYSIS]
Data show the synthetic effect of SNPs on the indices of adiposity and risk of obesity in Chinese girls, but failed to replicate the effect of five separate variants of SEC16B (show SEC16B Antibodies) rs10913469, SH2B1 rs4788102, PCSK1 (show PCSK1 Antibodies) rs6235, KCTD15 rs29941 and BAT2 (show BAT2 Antibodies) rs2844479.
Common variants near BDNF (show BDNF Antibodies) and SH2B1 show nominal evidence of association with snacking behavior in European populations.
rare missense mutations of FTO and SH2B1 did not confer risks of obesity in Chinese Han children in our cohort
SH2B1 in pancreatic beta-cells promotes insulin (show INS Antibodies) synthesis and secretion at least in part by enhancing activation of JAK2 (show JAK2 Antibodies) and/or Pdx1 (show PDX1 Antibodies) pathways in response to hormonal and nutritional signals.
hepatic SH2B1 is not required for the maintenance of normal insulin (show INS Antibodies) sensitivity and glucose metabolism; however, it regulates liver triacylglycerol synthesis, lipolysis, and VLDL secretion.
These data indicate that SH2B1 in beta-cells is an important prosurvival and proproliferative protein and promotes compensatory beta-cell expansion in the insulin (show INS Antibodies)-resistant state and in response to beta-cell stress.
SH2B1 is responsive to erythropoietin (show EPO Antibodies) stimulation and becomes phosphorylated
Leptin (show LEP Antibodies)-stimulated activation of hypothalamic JAK2 (show JAK2 Antibodies) and phosphorylation of hyphothalamic IRS2 (show IRS2 Antibodies) were significantly impaired in SH2B1(-/-) mice.
Mutations in the SH2 (show MYO15 Antibodies) domain of SH2B1 may increase the susceptibility to obesity and type 2 diabetes in a dominant-negative manner.
Genetic deletion of SH2B1 also resulted in growth retardation, obesity, and type 2 diabetes in mice; surprisingly, life span and oxidative resistance were reduced in SH2B1 null mice.
These results suggest that SH2-Bbeta regulation of Akt partly participates in the NGF-mediated development of allergic airway challenge.
These results suggest that 1) SH2-B beta specifically activates JAK2 (show JAK2 Antibodies), 2) APS (show SH2B2 Antibodies) negatively regulates both JAK2 (show JAK2 Antibodies) and JAK1 (show JAK1 Antibodies), and 3) both SH2-B beta and APS (show SH2B2 Antibodies) may serve as adapter proteins for all three JAKs independent of any role they have in JAK (show JAK3 Antibodies) activity.
This gene encodes a member of the SH2-domain containing mediators family. The encoded protein mediates activation of various kinases and may function in cytokine and growth factor receptor signaling and cellular transformation. Alternatively spliced transcript variants have been described.
SH2B adapter protein 1
, SH2B adaptor protein 1
, SH2B adapter protein 1-like
, SH2 domain-containing protein 1B
, SH2 domain-containing putative adapter SH2-B
, SH2-B signaling protein
, pro-rich, PH and SH2 domain-containing signaling mediator
, SH2-B PH domain containing signaling mediator 1
, SH2-B PH domain-containing signaling mediator 1
, fceRI gamma-chain-interacting protein SH2-B