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directly interacts with the ankyrin repeats of Shank; may be involved in regulating the function of Shank.
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Both Sharpin/Fas (show FAS ELISA Kits) and Sharpin/Fasl (show FASL ELISA Kits) compound mutant mice developed an auto-inflammatory phenotype similar to that seen in Sharpin null mice, indicating that initiation of apoptosis by FAS (show FAS ELISA Kits) signalling is likely not involved in the pathogenesis of this disease.
results altogether demonstrate distinct roles of SHARPIN in initiating systemic inflammation and dermatitis. Furthermore, skin inflammation in Sharpin(cpdm) mice is specifically modulated by IL-1beta (show IL1B ELISA Kits), highlighting the importance of specific targeted therapies in the IL-1 (show IL1A ELISA Kits) signaling blockade.
Itgb1 (show ITGB1 ELISA Kits) inhibition alleviates the chronic hyperproliferative dermatitis phenotype of Sharpin-deficient mice.
LUBAC components control TLR3 (show TLR3 ELISA Kits)-mediated innate immunity, thereby preventing development of immunodeficiency and autoinflammation.
Suppression of SHARPIN impaired cell proliferation, angiogenesis, and invasion and reduced levels of MMP-9 in P (show EPHB2 ELISA Kits)rost (show AKT1 ELISA Kits)ate cancer cells and reduced the size of Metastatic Lung tumors induced by these cells in mice.
Together, these data imply that SHARPIN regulates the normal invasive mammary gland branching morphogenesis in an epithelial cell extrinsic manner by controlling the organisation of the stromal extracellular matrix.
Study found that the NZF domain of SHARPIN, but not that of HOIL-1L (show RBCK1 ELISA Kits), is critical for effective protection from programmed cell death by enhancing the recruitment of the linear ubiquitin chain assembly complex to the activated TNFR (show TNFRSF1A ELISA Kits) complex. The binding activity to K63-linked ubiquitin chains that the NZF domain of SHARPIN, but not that of HOIL-1L (show RBCK1 ELISA Kits), possesses appears to be involved in the recruitment.
this study reveals a critical function of SHARPIN in TCR-induced NF-kappaB (show NFKB1 ELISA Kits) and JNK (show MAPK8 ELISA Kits) signalling and thymic Treg cell generation
SHARPIN-deficient mice develop a chronic proliferative dermatitis presenting angiogenesis and lymphatic dilatation.
Study identifies a role for SHARPIN in TCR signaling whereby it maintains immunological homeostasis and tolerance by regulating Treg cells.
Sharpin-Arp2 (show ACTR2 ELISA Kits)/3 interaction promotes lamellipodium formation.
The binding of SHARPIN or HOIL-1L (show RBCK1 ELISA Kits) facilitates the E2 loading of HOIP (show RNF31 ELISA Kits).
SIPL1 contributes to promote resistance to tamoxifen in Breast cancer cells through both AKT (show AKT1 ELISA Kits) and NF-kappaB (show NFKB1 ELISA Kits) actions.
the present study found that loss of the NEMO (show IKBKG ELISA Kits)-SHARPIN interaction impaired recruitment of truncated NEMO (show IKBKG ELISA Kits) forms into punctuate structures that are transiently formed on cell stimulation and thus led to a defect in linear ubiquitination
Overexpression of SHARPIN in Prostate cancer cells promoted cell growth and reduced apoptosis through NF-kB/ERK (show EPHB2 ELISA Kits)/Akt (show AKT1 ELISA Kits) pathway and apoptosis-associated proteins. SHARPIN enhances the metastasis of prostate cancer and impair patient survivals.
Our study firstly identifies the role of SHARPIN in promoting wild-type P53 (show TP53 ELISA Kits) degradation and correlates with poor prognosis in P53 (show TP53 ELISA Kits) wild-type breast cancer.
Data show that SHANK-associated RH domain interacting protein (SHARPIN) gene expression in breast cancer patients predicts clinical outcomes.
the roles of SHARPIN in inhibiting integrin activity and supporting linear ubiquitination are (molecularly) distinct.
progesterone significantly reduced SIPL1 mRNA and protein expression in MCF7 cells. As progesterone enhances breast cancer tumorigenesis in context dependent manner, inhibition of SIPL1 expression may contribute to progesterone's non-tumorigenic function
directly interacts with the ankyrin repeats of Shank; may be involved in regulating the function of Shank
, protein kinase C-interacting protein RBCC like 1
, shank-associated RH domain-interacting protein
, shank-interacting protein-like 1
, SHANK-associated RH domain interacting protein
, shank-interacting protein