Disease relevance of CISH

• We report here the absence of CIS expression in T lymphoma LSTRA that overexpresses the Lck protein tyrosine kinase and exhibits elevated STAT5 activity [1].
• Transfection of the adenovirus vector expressing cytokine-inducible SH2 containing protein 1 had no effect on signal transducers and activators of transcription 1, 3, and 6 signaling in normal keratinocytes [2].
• We examined the expression of SOCS genes in 17 breast carcinomas and 10 breast cancer lines, in comparison with normal tissue and breast lines [3].
• We report elevated expression of SOCS-1-3 and CIS immunoreactive proteins within in situ ductal carcinomas and infiltrating ductal carcinomas relative to normal breast tissue [3].
• The suppressor of cytokine-signaling (SOCS) protein, in particular SOCS-3, was shown as a leptin-regulated inhibitor of proximal leptin signaling, although its role during obesity remains uncertain [4].

Psychiatry related information on CISH

• In this study, the effect of MK-801 on various behaviours of bank voles, and in particular the relationship between CIS and PHIS, was investigated by repeated administration of MK-801 to stereotyping (ST) and non-stereotyping (NST) voles [5].
• Significant predictors of good speech perception included greater nonverbal intelligence, smaller family size, longer use of the updated SPEAK/CIS processing strategy, a fully active electrode array, greater electrical dynamic range between threshold and maximum comfort level, and greater growth of loudness with increasing stimulus intensity [6].
• METHODS: In employees with very low or very high fatigue levels, psychometrics of the Penn State Worry Questionnaire (PSWQ; measuring pathological worry) and the Checklist Individual Strength (CIS; measuring fatigue) were examined and their cross-sectional and longitudinal associations were explored [7].
• Neurogenic erectile dysfunction was considered in the remaining 4 patients (4.4%) with a positive response to the CIS test, abnormal findings on NPT monitoring, and a normal vascular system with color Doppler ultrasound [8].
• CASE STUDY: INTESTINAL OBSTRUCTION: Graduate Health Systems, a multisite integrated provider in the Philadelphia area, has used CADU/CIS to improve quality problems, reduce treatment-intensity variations, and improve clinical participation in care process evaluation and decision making [9].

High impact information on CISH

• The CIS family of proteins (also referred to as the SOCS or SSI family) has been implicated in the regulation of signal transduction by a variety of cytokines [10].
• These findings suggest mechanisms that regulate the assembly and activity of Cul5 E3 complexes through phosphorylation or autoubiquitination of the SOCS-box protein, and identify interactions between Vif and host cell proteins that may be therapeutic targets [11].
• In this SOCS box, alanine replaces the consensus cysteine in the previously identified SOCS box [12].
• This new motif was necessary but insufficient for interaction with Cul5-ElonginB-ElonginC, as two highly conserved Cys residues outside the SOCS box were required to interact with Cul5 but not ElonginC [12].
• The suppressors of cytokine signaling (SOCS) and cytokine-inducible SH2 protein are key physiological regulators of the immune system [13].

Chemical compound and disease context of CISH

• Aberrant methylation of these SOCS genes correlated with transcriptional silencing in ovarian and breast cancer cell lines, since expression was induced by the demethylating agent 5-azadeoxycytidine [14].
• In order to elucidate the role of the membrane adenosine triphosphate binding cassette-transporter cMOAT (canalicular multispecific anion transporter) (MRP2/ABCC2) in cisplatin resistance of melanoma, the expression of this protein was analyzed in the platinum drug-resistant cell line MeWo CIS 1 [15].
• To date, the majority of experience with the medical management of CIS of the bladder is with chemotherapeutic agent doxorubicin and the immunotherapeutic agent BCG [16].
• A study on the in vitro sensitivity of tumour cells from patients with ovarian cancer has been carried out in parallel with a clinical study designed to evaluate the role of high-dose cis-platinum (CIS) as first-line chemotherapy [17].
• The role of estrogen as a promoter agent of sporadic breast cancer has been considered by assaying, in benign breast disease (BBD) and in situ carcinomas (CIS), 2 markers, the estrogen receptor alpha (ERalpha) and cathepsin D (cath-D) involved in estrogen action on mammary tissue [18].

Biological context of CISH

• Suppressors of cytokine signaling (SOCS) proteins are stimulated in response to cytokine-inducible STAT phosphorylation, acting in a negative-feedback mechanism to hinder cytokine receptor activity [19].
• Comparison with cytokine-dependent BaF3 cells stimulated with interleukin-3 (IL-3) further reveals that CIS induction correlates with specific STAT5b post-translational modifications [1].
• In the present study, a novel human cDNA (CIS1b) which proved to be a variant of CIS1 gene was isolated by screen human placenta lambda gt11 cDNA library and 5'-rapid amplification of cDNA ends (RACE) [20].
• Furthermore, the gene structure of CIS1 was determined by comparing the cDNA sequences of CIS1 and CIS1b to the genomic sequence in human chromosome 3p21 [20].
• Cloning and characterization of CIS 1b (cytokine inducible SH2-containing protein 1b), an alternative splicing form of CIS 1 gene [20].

Anatomical context of CISH

• Expression of SOCS genes in normal and leukemic human leukocytes stimulated by prolactin, growth hormone and cytokines [21].
• The inhibition of growth hormone (GH) signaling by five members of the GH-inducible suppressor of cytokine signaling (SOCS/CIS) family was investigated in transfected COS cells [22].
• We investigated the mechanism regulating signal transducers and activators of transcription and the suppressor of cytokine signaling/cytokine-inducible SH2 containing protein family in keratinocytes, one of the major target cells for cytokines [2].
• There was no significant difference in expression of CIS and SOCS1 in microvessel endothelial cells [23].
• PRL induced iNOS and CIS mRNA expression in granulocytes [24].

Associations of CISH with chemical compounds

• Unlike CIS, SOCS-3 was rapidly tyrosine phosphorylated in response to IL-2 [25].
• Although a functional SH2 binding domain of CIS was not required for its interaction with IL-2Rbeta in vitro, its phosphotyrosine binding capability was essential for the inhibitory action of CIS [26].
• We have devised a protocol to generate probes for CISH that can be applied to formalin-fixed, paraffin-embedded tissue sections (FFPETS) [27].
• Furthermore, in lethally irradiated mice reconstituted with bone marrow infected by a tetracycline-regulated, SOCS-expressing lentiviral vector, doxycycline treatment promoted rapid, extensive precursor mobilization to the periphery [28].
• Vif binding to EloC is negatively regulated by serine phosphorylation in the BC-box motif of the SOCS-box [11].

Regulatory relationships of CISH

• Thus, we demonstrate that CIS can negatively control at least two independent IL-2 signaling pathways [26].
• Interleukin-4 upregulated the suppressor of cytokine signaling 1/JAB and cytokine-inducible SH2 containing protein 1 mRNA, with 3.4-fold and 5.1-fold increases in mRNA observed at 1 h post-interleukin-4, respectively [2].

Other interactions of CISH

• Inhibition of PRL hormone signaling by suppressor of cytokine signaling (SOCS)/cytokine-inducible SH2-containing protein (CIS) was investigated in transfected HEK 293 cells [29].
• Characterization of STAT5B phosphorylation correlating with expression of cytokine-inducible SH2-containing protein (CIS) [1].
• Several members, including CIS (cytokine-inducible SH2 protein), SOCS1 and SOCS3, are induced rapidly upon cytokine receptor activation and function in a negative-feedback loop, attenuating signalling at the receptor level [30].
• CIS is also a well-known target gene of signal transducer and activator of transcription 5 (STAT5) pathways, providing normal negative feedback control of signaling by cytokines and growth factors [1].
• Isolated RNA was subjected to semiquantitative reverse transcriptase polymerase chain reaction analysis of CIS/JAB expression [31].
• A non-overlapping recruitment pattern is observed for SOCS2 and CIS with positions Y487 and Y595 as major binding sites, ruling out SOCS-mediated inhibition of STAT5 activation by competition for shared binding sites [32].

Analytical, diagnostic and therapeutic context of CISH

• 3. The expression patterns of CIS1b as well as CIS1 were analysed by Northern blot [20].
• Hypophysectomy reduced the levels of SOCS-2 and CIS mRNA in liver, muscle, and fat, whereas SOCS-3 expression was unchanged [33].
• Chromogenic (CISH) and fluorescent (FISH) in situ hybridization have emerged as reliable techniques to identify amplifications and chromosomal translocations [27].
• HER2 expression can be determined through IHC, FISH, CISH and ELISA among other tests, with reported positivity frequencies of overexpression varying from 1.8% to 76% [34].
• The gene copy numbers of REST were investigated by chromogenic (CISH) and fluorescence in situ hybridization (FISH) techniques [35].

References