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Miles Phillips
Miles Phillips

Vice City Nude Mod

Not to be lazy but I saw the VC Nude mod which makes 48 female models in the game partially nude. I know you have to use IMGtools for it to work, but which files on the gta3.IMG are for the stippers for the Pole Position strip club? I just want to put the nude skin for them ONLY and not for anyone else.

Vice City Nude Mod

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Last week we told you about Lustful Illumination, a website that provided user-made modifications that undress the characters in Dead or Alive 5: Last Round. The nude mods were released on the same day the fighting game launched on PC, and after publisher Koei Tecmo specifically warned players to be "good and moral" and not modify the fighting game to create nude versions of its characters.

How long have you been creating nude mods? How did you get into this?Ever since I was young, I enjoyed to play a lot of computer games. One of the games was the first Sims. One day, just for fun, I explored the installation folders of the game and stumbled upon pictures that looked weird. On them you can see parts of the Sims. Like their clothing, skin, and hair. So I thought, if I edit such an image, it could also appear changed in the game. Thrilled by this thought, I opened up the good old MS Paint and started altering some pixels of one of the game's images. After I saved it, I started the game and saw that it worked. That was my first modification for a computer game ever! It was so exciting that I never gave up modding. I'm not sure, but I think I've been making nudemods for about 8-10 years now.

How did you manage to release the skins/mods on the same day the game was released on PC?While it was fun modding DOA5, it was a pain at the same time because it took the whole night to make that mod. A great help was Rathren, a friend that I know from Game Vixen Zone. Game Vixen Zone is the forum that I use the most regarding all the nudemod stuff. Rathren did not only helped me with some modding work, he also motivated me to get this job done without any sleep. We were both really tired as I uploaded the mod on my website early in the morning. It took only about one hour for the first article about my nudemod to appear. That caused a lot of traffic on my website. It was a great experience to see that happen. The only thing that keeps me making more nudemods for Dead or Alive 5 is the feedback of all the cool people that sent me a lot of comments and even donations.

Did you see that the producers of Dead or Alive 5 asked people not to create nude mods and to be "good and moral?"Oh yes, I saw that and I laughed very hard. I don't know the real reason why they've made that comment. Maybe just because that statement would spread around the internet and increase their profit. Or maybe they really mean what they say, who knows. But the thing is, that some of my nudemods for Dead or Alive 5 require a certain official DLC [extra piece of downloadable content] for that game that you have to buy for money. A LOT of money. How can a DLC be that expensive anyway!? Well, as you see my and others' nudemods increase their profit as well.

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Note: Pictures of Hot Sex Woman, No Images files are hosted on our server, We only help to make it easier for visitors to find a Porn pics, nude sex photos and XXX Photos in some search engines. Hot Sex Picture is not responsible for third party website content. If one of this file is your intelectual property (copyright infringement) or child pornography / immature sounds, please send report to abuse.

Amateur hardcore clips of the month:The caveat, however, is that everything on the site appears vice city nude mod on this one page. It may appear jumbled, but it's all here and accounted for (i think). As always, please email me if you have any questions/comments/complains/submissions/reports of broken links/etc/etc.

All models were at least 18 years old when they were photographed. We have a zero-tolerance policy against illegal pornography.All content on this site provided by 3rd parties. We take no responsibility for "Vice city nude mod porn scenes" and any content on this website.

Certain inherited progressive neurodegenerative disorders, such as spinocerebellar ataxia (SCA), affect neurons in large areas of the central nervous system (CNS). The selective expression of disease-causing and therapeutic genes in susceptible regions and cell types is critical for the generation of animal models and development of gene therapies for these diseases. Previous studies have demonstrated the advantages of the short synapsin I (SynI) promoter (0.5 kb) as a neuron-specific promoter for robust transgene expression. However, the short SynI promoter has also shown some promoter activity in glia and a lack of transgene expression in significant areas of the CNS. New methods: To improve the SynI promoter, we used a SynI promoter that is twice as long (1.0 kb) as the short SynI promoter and incorporated a minimal CMV (minCMV) sequence. We observed that the 1.0 kb rat SynI promoter with minCMV [rSynI(1.0)-minCMV] exhibited robust promoter strength, excellent neuronal specificity and wide-ranging transgene expression throughout the CNS. Comparison with existing methods: Compared with the two previously reported short (0.5 kb) promoters, the new promoter was superior with respect to neuronal specificity and more efficiently transduced neurons. Moreover, transgenic mice expressing the mutant protein ATXN1[Q98], which causes SCA type 1 (SCA1), under the control of the rSynI(1.0)-minCMV promoter showed robust transgene expression specifically in neurons throughout the CNS and exhibited progressive ataxia. rSynI(1.0)-minCMV drives robust and neuron-specific transgene expression throughout the CNS and is therefore useful for viral vector-mediated neuron-specific gene delivery and generation of neuron-specific transgenic animals. Copyright 2013 Elsevier B.V. All rights reserved.

TFII-I proteins are ubiquitously expressed transcriptional factors involved in both basal transcription and signal transduction activation or repression. TFII-I proteins are detected as early as at two-cell stage and exhibit distinct and dynamic expression patterns in developing embryos as well as mark regional variation in the adult mouse brain. Analysis of atypical small and rare chromosomal deletions at 7q11.23 points to TFII-I genes (GTF2I and GTF2IRD1) as the prime candidates responsible for craniofacial and cognitive abnormalities in the Williams-Beuren syndrome. TFII-I genes are often subjected to alternative splicing, which generates isoforms that show different activities and play distinct biological roles. The coding regions of TFII-I genes are composed of more than 30 exons and are well conserved among vertebrates. However, their 5' untranslated regions are not as well conserved and all poorly characterized. In the present work, we analyzed promoter regions of TFII-I genes and described their additional exons, as well as tested tissue specificity of both previously reported and novel alternatively spliced isoforms. Our comprehensive analysis leads to further elucidation of the functional heterogeneity of TFII-I proteins, provides hints on search for regulatory pathways governing their expression, and opens up possibilities for examining the effect of different haplotypes on their promoter functions.

Mammalian target of rapamycin (mTOR) is a core component of raptor-mTOR (mTORC1) and rictor-mTOR (mTORC2) complexes that control diverse cellular processes. Both mTORC1 and mTORC2 regulate several elements downstream of type I insulin-like growth factor receptor (IGF-IR) and insulin receptor (InsR). However, it is unknown whether and how mTOR regulates IGF-IR and InsR themselves. Here we show that mTOR possesses unexpected tyrosine kinase activity and activates IGF-IR/InsR. Rapamycin induces the tyrosine phosphorylation and activation of IGF-IR/InsR, which is largely dependent on rictor and mTOR. Moreover, mTORC2 promotes ligand-induced activation of IGF-IR/InsR. IGF- and insulin-induced IGF-IR/InsR phosphorylation is significantly compromised in rictor-null cells. Insulin receptor substrate (IRS) directly interacts with SIN1 thereby recruiting mTORC2 to IGF-IR/InsR and promoting rapamycin- or ligand-induced phosphorylation of IGF-IR/InsR. mTOR exhibits tyrosine kinase activity towards the general tyrosine kinase substrate poly(Glu-Tyr) and IGF-IR/InsR. Both recombinant mTOR and immunoprecipitated mTORC2 phosphorylate IGF-IR and InsR on Tyr1131/1136 and Tyr1146/1151, respectively. These effects are independent of the intrinsic kinase activity of IGF-IR/InsR, as determined by assays on kinase-dead IGF-IR/InsR mutants. While both rictor and mTOR immunoprecitates from rictor(+/+) MCF-10A cells exhibit tyrosine kinase activity towards IGF-IR and InsR, mTOR immunoprecipitates from rictor(-/-) MCF-10A cells do not induce IGF-IR and InsR phosphorylation. Phosphorylation-deficient mutation of residue Tyr1131 in IGF-IR or Tyr1146 in InsR abrogates the activation of IGF-IR/InsR by mTOR. Finally, overexpression of rictor promotes IGF-induced cell proliferation. Our work identifies mTOR as a dual-specificity kinase and clarifies how mTORC2 promotes IGF-IR/InsR activation. 350c69d7ab


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