Tsc2 (Phospho_Ser1254) Antibody
- Known as:
- Tsc2 (Phospho_Ser1254) Antibody
- Catalog number:
- E012048-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- Tsc2 (Phospho_Ser1254) Antibody
Related genes to: Tsc2 (Phospho_Ser1254) Antibody
- Gene:
- TSC2 NIH gene
- Name:
- TSC complex subunit 2
- Previous symbol:
- TSC4
- Synonyms:
- tuberin, LAM, PPP1R160
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-25
- Date modifiied:
- 2019-04-23
Related products to: Tsc2 (Phospho_Ser1254) Antibody
Related articles to: Tsc2 (Phospho_Ser1254) Antibody
- Tuberous sclerosis complex (TSC) is a rare autosomal dominant neurodevelopmental disorder caused by loss-of-function mutations in or , resulting in chronic hyperactivation of the mechanistic target of rapamycin (mTOR) pathway. TSC patients experience a wide spectrum of cognitive, behavioral, and psychiatric features collectively termed Tuberous Sclerosis Complex Associated Neuropsychiatric Disorders (TAND). Moreover, these patients develop a clinical trajectory in adulthood with clinical and neuropathological features overlapping those of Alzheimer's disease (AD). Prior neuropathological studies have shown accumulation of AD-type mixed 3R/4R tau isoforms in adults with TSC that is amyloid-independent. - Source: PubMed
Publication date: 2026/09/11
Baumel JocelynLutz MichaelDing CynthiaCapal JamieRitter DavidKrueger DarcySalter AliceWerner KlausLiu Andy J - Tuberous Sclerosis Complex (TSC) is caused by inactivating mutations in either the or genes, leading to activation of the mammalian target of rapamycin complex 1 (mTORC1) and unhindered cell growth and proliferation. The epithelium of TSC renal cysts in both mice and humans is composed of proliferating A-intercalated (A-IC) cells. The exact molecular mechanism of kidney cystogenesis in TSC remains speculative. - Source: PubMed
Publication date: 2026/09/23
Barone SharonZahedi KamyarSoleimani Manoocher - The nutrient-sensing mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway controls cellular and organismal growth and metabolism, and aberrant activation is linked to human disease, including metabolic disease. Cellular studies have established regulatory mechanisms influencing mTORC1 activation, but the physiological signals that control mTORC1 at the organismal and tissue levels are less well-defined. mTORC1 is dynamically regulated by fasting and feeding in metabolic tissues, with both nutrients and insulin proposed to activate mTORC1 in response to feeding. Here, studies employing a liver-specific genetic mouse model demonstrate that AKT-mediated TSC2 phosphorylation is the predominant mechanism of hepatic mTORC1 induction by insulin but is dispensable for activation by feeding. Furthermore, postprandial activation of hepatic mTORC1 requires dietary protein, which dictates the insulin-responsiveness of the pathway. Contrary to dogma, hepatic mTORC1 signaling was not elevated in response to diet-induced obesity, despite overt impairments in insulin and glucose homeostasis, and blocking hepatic AKT-TSC-mTORC1 signaling did not affect these metabolic phenotypes. Evidence is also provided supporting a role for glucagon in hepatic mTORC1 suppression during fasting. This study reveals a hierarchy of physiological signals regulating hepatic mTORC1. - Source: PubMed
Publication date: 2026/08/31
Kalafut Krystle CCormerais YannCissé Madi YLapp Samuel CInouye Karen EHotamışlıgil Gökhan SManning Brendan D - Cervical cancer remains a major global health burden and is predominantly associated with human papillomavirus (HPV) infection. However, a subset of tumors develops independently of HPV, and their molecular characteristics are not fully understood. This study aimed to synthesize and compare the frequency of somatic mutations across key oncogenic pathways, p53, PI3K-Akt-mTOR, AMPK, and Ras-Raf-MAPK, in HPV-associated and HPV-independent cervical cancers. - Source: PubMed
Publication date: 2026/09/01
Santos Ana Beatriz CamilloCarobeli Lucimara RodriguesMeirelles Lyvia Eloiza De FreitasDe Souza Maria Vitória FelipeDa Silva Vânia Ramos SelaConsolaro Marcia Edilaine Lopes - The natural history of pancreatic neuroendocrine tumors (NETs) can span decades of slow progression, but it is unpredictable, with a more aggressive course also being common. The two clinical biomarkers currently used to define the grade of a tumor, the Ki67 index and the mitotic index, are not able to fully capture the course of individual patients. This creates an unmet need to discover better prognostic biomarkers to inform therapeutic decisions, as well as therapies with overall survival benefit. Two genomic series of pancreatic NETs were examined to discover sub-sets with divergent characteristics. Primary data were downloaded from the cBioportal cancer genomics portal and analyzed at the individual sample level. Pancreatic NET patients without // mutations were younger than NET patients with any of these mutations. Pancreatic NETs had consistently low tumor mutation burden but were heterogeneous in their Fraction Genome Altered (FGA), a metric of chromosomal instability (CIN), with one group presenting high FGA and another possessing low to intermediate FGA. FGA did not correlate with Ki67, but high FGA was most prevalent in cases with mutations in and or . mutations were significantly more prevalent in the group with high FGA. - Source: PubMed
Publication date: 2026/09/08
Voutsadakis Ioannis A